To struggle for survival, all living organisms, from protists to humans, must defend themselves f... more To struggle for survival, all living organisms, from protists to humans, must defend themselves from attack by predators. From the time when life began around 3,500 million years ago, all living cells have evolved mechanisms and strategies to optimally defend themselves, while the invaders also need to survive by evading these immune defenses. The end results would be healthy co-evolution of both parties. Classically, immune host defense is divided into two main categories, namely, innate and adaptive systems. It is well documented that while vertebrates possess both systems, invertebrates and prokaryotes like bacteria and archaea depend almost exclusively on the innate immune functions. Although the adaptive immune system like antibodies and cellular immunity or their equivalents are believed to have evolved at the time when the vertebrates first appeared about 550 million years ago, more recent information from molecular and genomic studies suggest that different forms of adaptive immune system may also be present in the invertebrates as well. These forms of "adaptive" immune system exhibit, for instance, limited degrees of memory, diversity and similarities of their immune receptors with the immunoglobulin domains of the conventional adaptive immune system of vertebrates. Organized lymphoid tissues have been identified in all vertebrates. Very recent molecular and genetic data further suggest that a special type of adaptive system functioning like RNAi of vertebrates is also present in the very ancient form of life like the bacteria and archaea. In this review, I provide some insights, based on recent information gathering from evolutionary data of innate and adaptive immune receptors of invertebrate and vertebrate animals that should convince the readers that our current view on the innate and adaptive immunity may need to be modified. The distinction between the two systems should not be thought of in terms of a "black and white" phenomenon anymore, as recent molecular and genomic information points to the fact that a line of distinction is not as sharp as it was once thought to be, but it is blurred by different shades of grey.
Innate and adaptive immune systems consist of cells and molecules that work together in concert t... more Innate and adaptive immune systems consist of cells and molecules that work together in concert to fight against microbial infection and maintain homeostasis. Hosts encounter microbes / exogenous pathogen-associated molecular patterns (PAMPs) and endogenous damage-associated molecular patterns (DAMPs) all the time and they must have proper mechanisms to counteract the danger such that appropriate responses (e.g., degree of inflammation and types of mediators induced) can be mounted in different scenarios. Increasing numbers of endogenous danger signals of host origin are being identified including, for example, uric acid and cholesterol crystals, high mobility group box1 (HMGB1) protein, oxidized LDL, vesicans, heat shock proteins (HSPs) and self DNA. Many of these endogenous ligands have been shown to be associated with inflammation-related diseases like atherosclerosis, gout and type 2 diabetes. Several DAMPs appear to have the ability to interact with more than one receptor. We are now beginning to understand how the immune system can distinguish infection from endogenous ligands elaborated following cellular insults and tissue damage. Appropriate responses to maintain the homeostatic state in health and disease depend largely on the recognition and response to these stimuli by germline encoded pattern-recognition receptors (PRRs) present on both immune and non-immune cells. These receptors are, for example, Toll-like receptors (TLRs), C-type lectin receptors (CLRs) and cytosolic receptors (e.g., RLRs, NLRs and some intracellular DNA sensors). Atypical PRR "danger" receptors, like the receptor for advanced glycation end products (RAGE) and their ligands have been identified. A proper response to maintain homeostasis relies on specific negative regulators and regulatory pathways to dampen its response to tissue injury while maintaining the capacity to eliminate infection and induce proper tissue repair. Moreover, some PRRs (e.g., TLR2,TLR4 and NLRP3) and atypical PRRs can recognize both PAMPs and DAMPs, either as single entities or after forming complexes (e.g., immune complexes, or DNA- HMGB1 and DNA-LL37 complexes), so there must be a mechanism to selectively depress or alleviate the inflammatory response to DAMPs, while leaving that of PAMPs intact. Excessive inflammatory responses can induce considerable tissue damage and can be highly detrimental to the host. For example, CD24 reacting with HMGB1 and HSPs has been implicated to function as negative regulator for RAGE. In this review, I will briefly overview the information on various host and microbial components and bring together the information to synthesize a model to explain how homeostasis can be maintained in states of health and disease. Understanding the molecular mechanisms by which the immune system functions under different scenarios will provide us with ways and means to design appropriate approaches, for example, to prevent or treat autoimmune and inflammatory diseases or the ability to design new drugs or formulate safe chemicals for vaccine adjuvants.
The effect of vitamin A on mucosal immunity has never been subjected to extensive studies until r... more The effect of vitamin A on mucosal immunity has never been subjected to extensive studies until recently. We started to work in this area in the early 1970s when we observed that children with protein-calorie malnutrition (PCM) often had defective mucosal immunity, judging from the incidence of respiratory tract infections and diarrhea. We reported that these children had depressed secretory IgA (sIgA) levels in their nasal wash fluids. The IgA level in specimens collected from those superimposed with some degrees of vitamin A deficiency state appeared to be more severely affected. In order to better understand the underlying mechanism associated with this condition, we started to study more detail the deficiency state using experimental vitamin A-deficient rats. From a series of experiments using this animal model, we proposed that vitamin A was needed for transport and/or secretion of sIgA across the mucosa. This conclusion was based on the observation that the secretory component of sIgA synthesized by the epithelial cells of these vitamin A deficient animals was adversely affected as compared to the control animals. From that time onward, much progress has been made by several other groups showing that other mechanisms could also influence the integrity and immune function of the mucosa. For instance, recent studies demonstrated that retinoic acid which is a biologically active form of vitamin A has an essential role in mucosal homeostasis, controlling tolerance and immunity in these non-lymphoid tissues. Such a conclusion was made possible by the availability of sophisticated new molecular biology and genetic engineering techniques together with advances in the field of immunoregulation, e.g., the discovery of dendritic cells (DCs) and T helper cell subsets in 1980s, and the role of Toll-like receptors (TLRs) together with other innate immune regulators in controlling adaptive immune response in the early 1990s. These advances provided considerable new insights into the pleiotropic roles of vitamin A including educating mucosal DCs, differentiation of lymphocyte lineages and imprinting them with mucosal-homing properties as well as in regulating tolerance and immunity. The identification of a novel lymphocyte subpopulation, innate lymphoid cells (ILCs), at the beginning of this century has provided us with an additional insight into a new role of vitamin A in regulating homeostasis at the mucosal surface through influencing ILCs. Another new player that regulates intestinal homeostasis and mucosal immune response is microbiota whose composition is known to vary with vitamin A status. So it appears now that the role of vitamin A on mucosal immunity is far beyond regulating the adaptive Th1-Th2 cell response, but is highly pleiotropic and more complicating, e.g., polarizing the phenotype of mucosal DCs and macrophages, directing gut-homing migration of T and B cells, inducing differentiation of effector T cells and Treg subpopulation, balancing mucosal ILCs subpopulation and influencing the composition of microbiota. In this review, I will attempt to bring together these important advances to provide a comprehensive and contemporary perspective on the role of vitamin A in regulating mucosal immunity.
The local immune system of children suffering protein-calorie malnutrition (PCM) was investigated... more The local immune system of children suffering protein-calorie malnutrition (PCM) was investigated by analyzing the amount of immunoglobulins in the nasal washing on admission, repeatedly during 84 days of hospital therapy, and on follow-up, one to two years later. Although measured concentrations of total protein, IgG, and albumin in nasal washings were reduced in children with PCM, only secretory IgA concentrations were significantly lower (P less than .01) in PCM compared to normal children. Mean secretory IgA concentrations were significantly reduced on admission through hospital day 70 and returned to near normal thereafter. At one to two years after hospital discharge, mean concentrations of secretory IgA in nasal secretions were within normal limits. The concentrations of secretory IgA in nasal washings were lowest at a time when serum IgA was markedly elevated; serum IgA concentrations fell to normal values during dietary treatment. The possible role of secretory IgA deficiency in PCM and infection is discussed.
BACKGROUND AND OBJECTIVE Female sex hormones are elevated and are potential host response modifie... more BACKGROUND AND OBJECTIVE Female sex hormones are elevated and are potential host response modifiers during pregnancy. Modulation of immune responses by estrogen and progesterone may be responsible for periodontal inflammation. Therefore, we aimed to investigate the role of β-estradiol and progesterone in human monocyte immune responses, at cellular and molecular levels, to identify their role as a possible immunological link between pregnancy and periodontal disease. MATERIAL AND METHODS Primary human monocytes were purified from human peripheral blood mononuclear cells by adherent method. Expression of Toll-like receptor (TLR) 2, 4 and CD14 was analyzed by flow cytometry. TLR2, TLR4, cyclooxygenase-2 (COX2), nuclear factor-kappa B (NF-κB) and NF-κB inhibitor-alpha mRNA expressions were measured using real-time reverse transcriptase-polymerase chain reaction and prostaglandin E2 secretion was assayed by enzyme-linked immunosorbent assay. NF-κB expression was also examined by immunofluorescence. Western blotting was performed to determine the activation of mitogen-activated protein kinase pathway. RESULTS We report herein that both β-estradiol and progesterone significantly reduced TLR2 expression at both protein and mRNA levels but had less of an effect on TLR4 expression in primary human monocytes. We also found that the hormones decreased monocyte cell surface protein expression of CD14. Significantly, β-estradiol and progesterone dose-dependently downregulated monocyte expression of COX2 mRNA. Pretreatment monocytes with β-estradiol or progesterone reduced effects of Porphyromonas gingivalis lipopolysaccharide (LPS) on COX2 mRNA expression and decreased prostaglandin E2 secretion by the monocytes. Furthermore, we demonstrated that both β-estradiol and progesterone inhibited P. gingivalis LPS-induced NF-κB signaling pathway through the upregulation of NF-κB inhibitor-alpha expression. However, neither β-estradiol nor progesterone altered the phosphorylation of the p38, the extracellular signal-regulated kinase 1/2 and the c-Jun N-terminal activated kinase in P. gingivalis LPS-stimulated monocytes. Thus, the inhibitory effects of these hormones on the response of human monocytes to P. gingivalis LPS appear to be independent on mitogen-activated protein kinase signaling pathway. CONCLUSION The results of the present study suggest that β-estradiol and progesterone could influence the immune response of human monocytes to periodontal pathogens and this process may have a role in the clinical manifestations of periodontal disease associated with pregnancy.
Monoclonal antibodies (MoAb) were produced against somatic antigens of adult human liver fluke Op... more Monoclonal antibodies (MoAb) were produced against somatic antigens of adult human liver fluke Opisthorchis viverrini. Earlier studies attached diagnostic potential to an 89-90 kD antigen present in both somatic extracts and in vitro culture supernatants as well as to the abundant 16-17 kD tegumental protein doublet. Mice made excellent immune responses to low dose somatic extract adsorbed onto nitrocellulose or to the 80-95 kD region of SDS gel Western blots. The antigen specificities of hybridomas reactive with somatic antigen by ELISA were determined by radioimmunoprecipitation or immunoblotting. Six MoAb reacted with the desired 16 kD tegumental protein. A 90 kD somatic protein was identified by 9 clones. By indirect immunofluorescence, monoclonals reactive with the 16 kD polypeptide identified the outermost surface of the tegument. The 90 kD antigen was associated with all major muscle systems, most strikingly the crossed subtegumental layers, oral and ventral suckers, pharynx and a thin layer surrounding caeca. The biochemical identity of this muscle-associated antigen is unknown, but it is clearly distinct from the previously identified species-specific 89 kD exoantigen. The 16 kD tegumental protein shares epitopes with a number of related flukes. However, 2 MoAb which react with this protein show no crossreaction.
Periodontitisisaninflammatorydiseaseinducedbybacterialinsultandhostimmuneresponse.�Epidemiologica... more Periodontitisisaninflammatorydiseaseinducedbybacterialinsultandhostimmuneresponse.�Epidemiological� and clinical studies over the past decade have suggested its association with development of atherogenesis, which may lead to cardiovascular disease and its complications. Lifestyle diseases are non-communicable chronic diseases of longevity that are increasing in frequency as countries become more industrialized and people live longer. The lifestyle diseases, including for example atherosclerosis, cardiovascular diseases, stroke, type 2 diabetes mellitus, obesity and osteoporosis, are at present increasing at an alarming rate worldwide, and are related largely to diet and thewayapersonlives.�Thelongofficehourandthetypeofactivitiesweencounterdailyinourofficemakeusinthe� dental professions are at risk for developing lifestyle diseases. Healthy lifestyle factors include good nutrition, regular exercise, non-smoking and body mass index of less than 25 kg/m 2 , etc. Because the oral cavit...
Beneficial effects of Va and/or Zn supplementation of children in NE Thailand are described in a ... more Beneficial effects of Va and/or Zn supplementation of children in NE Thailand are described in a companion abstract. In the same study, blastogenic response (BR) of T-lymphocytes to concanavalin-A (ConA) and PPD were assayed in cultures containing mononuclear cells (MNC) or whole blood (WB). Methods were previously described. Children were previously vaccinated with BCG. BR to ConA of MNC or
Monoclonal antibodies (MoAb) were produced against a major soluble metabolic product (excretory-s... more Monoclonal antibodies (MoAb) were produced against a major soluble metabolic product (excretory-secretory, ES) of Opisthorchis viverrini. The latter was obtained in a form of spent culture medium in which the adult flukes had been maintained in vitro. The MoAb produced were exclusively associated with either IgG or IgM isotypes. When screened against a panel of parasite antigens by indirect ELISA, these MoAb exhibited three patterns of reactivity. Approximately 50% of the MoAb were highly specific for O. viverrini and another 25% cross-reacted only with Clonorchis sinensis. The remaining 25% cross-reacted extensively with other parasites. Results from radioimmunoprecipitation and immunoblotting experiments showed all MoAb to react with the 89-kDa glycoprotein. By indirect immunofluorescence, these MoAb reacted almost exclusively with the tegumental surface, tegumental cells, cecum and developing miracidium. Different lines of evidence suggest that these MoAb reacted with different epitopes on the same 89-kDa polypeptide carrier.
To struggle for survival, all living organisms, from protists to humans, must defend themselves f... more To struggle for survival, all living organisms, from protists to humans, must defend themselves from attack by predators. From the time when life began around 3,500 million years ago, all living cells have evolved mechanisms and strategies to optimally defend themselves, while the invaders also need to survive by evading these immune defenses. The end results would be healthy co-evolution of both parties. Classically, immune host defense is divided into two main categories, namely, innate and adaptive systems. It is well documented that while vertebrates possess both systems, invertebrates and prokaryotes like bacteria and archaea depend almost exclusively on the innate immune functions. Although the adaptive immune system like antibodies and cellular immunity or their equivalents are believed to have evolved at the time when the vertebrates first appeared about 550 million years ago, more recent information from molecular and genomic studies suggest that different forms of adaptive immune system may also be present in the invertebrates as well. These forms of "adaptive" immune system exhibit, for instance, limited degrees of memory, diversity and similarities of their immune receptors with the immunoglobulin domains of the conventional adaptive immune system of vertebrates. Organized lymphoid tissues have been identified in all vertebrates. Very recent molecular and genetic data further suggest that a special type of adaptive system functioning like RNAi of vertebrates is also present in the very ancient form of life like the bacteria and archaea. In this review, I provide some insights, based on recent information gathering from evolutionary data of innate and adaptive immune receptors of invertebrate and vertebrate animals that should convince the readers that our current view on the innate and adaptive immunity may need to be modified. The distinction between the two systems should not be thought of in terms of a "black and white" phenomenon anymore, as recent molecular and genomic information points to the fact that a line of distinction is not as sharp as it was once thought to be, but it is blurred by different shades of grey.
Innate and adaptive immune systems consist of cells and molecules that work together in concert t... more Innate and adaptive immune systems consist of cells and molecules that work together in concert to fight against microbial infection and maintain homeostasis. Hosts encounter microbes / exogenous pathogen-associated molecular patterns (PAMPs) and endogenous damage-associated molecular patterns (DAMPs) all the time and they must have proper mechanisms to counteract the danger such that appropriate responses (e.g., degree of inflammation and types of mediators induced) can be mounted in different scenarios. Increasing numbers of endogenous danger signals of host origin are being identified including, for example, uric acid and cholesterol crystals, high mobility group box1 (HMGB1) protein, oxidized LDL, vesicans, heat shock proteins (HSPs) and self DNA. Many of these endogenous ligands have been shown to be associated with inflammation-related diseases like atherosclerosis, gout and type 2 diabetes. Several DAMPs appear to have the ability to interact with more than one receptor. We are now beginning to understand how the immune system can distinguish infection from endogenous ligands elaborated following cellular insults and tissue damage. Appropriate responses to maintain the homeostatic state in health and disease depend largely on the recognition and response to these stimuli by germline encoded pattern-recognition receptors (PRRs) present on both immune and non-immune cells. These receptors are, for example, Toll-like receptors (TLRs), C-type lectin receptors (CLRs) and cytosolic receptors (e.g., RLRs, NLRs and some intracellular DNA sensors). Atypical PRR "danger" receptors, like the receptor for advanced glycation end products (RAGE) and their ligands have been identified. A proper response to maintain homeostasis relies on specific negative regulators and regulatory pathways to dampen its response to tissue injury while maintaining the capacity to eliminate infection and induce proper tissue repair. Moreover, some PRRs (e.g., TLR2,TLR4 and NLRP3) and atypical PRRs can recognize both PAMPs and DAMPs, either as single entities or after forming complexes (e.g., immune complexes, or DNA- HMGB1 and DNA-LL37 complexes), so there must be a mechanism to selectively depress or alleviate the inflammatory response to DAMPs, while leaving that of PAMPs intact. Excessive inflammatory responses can induce considerable tissue damage and can be highly detrimental to the host. For example, CD24 reacting with HMGB1 and HSPs has been implicated to function as negative regulator for RAGE. In this review, I will briefly overview the information on various host and microbial components and bring together the information to synthesize a model to explain how homeostasis can be maintained in states of health and disease. Understanding the molecular mechanisms by which the immune system functions under different scenarios will provide us with ways and means to design appropriate approaches, for example, to prevent or treat autoimmune and inflammatory diseases or the ability to design new drugs or formulate safe chemicals for vaccine adjuvants.
The effect of vitamin A on mucosal immunity has never been subjected to extensive studies until r... more The effect of vitamin A on mucosal immunity has never been subjected to extensive studies until recently. We started to work in this area in the early 1970s when we observed that children with protein-calorie malnutrition (PCM) often had defective mucosal immunity, judging from the incidence of respiratory tract infections and diarrhea. We reported that these children had depressed secretory IgA (sIgA) levels in their nasal wash fluids. The IgA level in specimens collected from those superimposed with some degrees of vitamin A deficiency state appeared to be more severely affected. In order to better understand the underlying mechanism associated with this condition, we started to study more detail the deficiency state using experimental vitamin A-deficient rats. From a series of experiments using this animal model, we proposed that vitamin A was needed for transport and/or secretion of sIgA across the mucosa. This conclusion was based on the observation that the secretory component of sIgA synthesized by the epithelial cells of these vitamin A deficient animals was adversely affected as compared to the control animals. From that time onward, much progress has been made by several other groups showing that other mechanisms could also influence the integrity and immune function of the mucosa. For instance, recent studies demonstrated that retinoic acid which is a biologically active form of vitamin A has an essential role in mucosal homeostasis, controlling tolerance and immunity in these non-lymphoid tissues. Such a conclusion was made possible by the availability of sophisticated new molecular biology and genetic engineering techniques together with advances in the field of immunoregulation, e.g., the discovery of dendritic cells (DCs) and T helper cell subsets in 1980s, and the role of Toll-like receptors (TLRs) together with other innate immune regulators in controlling adaptive immune response in the early 1990s. These advances provided considerable new insights into the pleiotropic roles of vitamin A including educating mucosal DCs, differentiation of lymphocyte lineages and imprinting them with mucosal-homing properties as well as in regulating tolerance and immunity. The identification of a novel lymphocyte subpopulation, innate lymphoid cells (ILCs), at the beginning of this century has provided us with an additional insight into a new role of vitamin A in regulating homeostasis at the mucosal surface through influencing ILCs. Another new player that regulates intestinal homeostasis and mucosal immune response is microbiota whose composition is known to vary with vitamin A status. So it appears now that the role of vitamin A on mucosal immunity is far beyond regulating the adaptive Th1-Th2 cell response, but is highly pleiotropic and more complicating, e.g., polarizing the phenotype of mucosal DCs and macrophages, directing gut-homing migration of T and B cells, inducing differentiation of effector T cells and Treg subpopulation, balancing mucosal ILCs subpopulation and influencing the composition of microbiota. In this review, I will attempt to bring together these important advances to provide a comprehensive and contemporary perspective on the role of vitamin A in regulating mucosal immunity.
The local immune system of children suffering protein-calorie malnutrition (PCM) was investigated... more The local immune system of children suffering protein-calorie malnutrition (PCM) was investigated by analyzing the amount of immunoglobulins in the nasal washing on admission, repeatedly during 84 days of hospital therapy, and on follow-up, one to two years later. Although measured concentrations of total protein, IgG, and albumin in nasal washings were reduced in children with PCM, only secretory IgA concentrations were significantly lower (P less than .01) in PCM compared to normal children. Mean secretory IgA concentrations were significantly reduced on admission through hospital day 70 and returned to near normal thereafter. At one to two years after hospital discharge, mean concentrations of secretory IgA in nasal secretions were within normal limits. The concentrations of secretory IgA in nasal washings were lowest at a time when serum IgA was markedly elevated; serum IgA concentrations fell to normal values during dietary treatment. The possible role of secretory IgA deficiency in PCM and infection is discussed.
BACKGROUND AND OBJECTIVE Female sex hormones are elevated and are potential host response modifie... more BACKGROUND AND OBJECTIVE Female sex hormones are elevated and are potential host response modifiers during pregnancy. Modulation of immune responses by estrogen and progesterone may be responsible for periodontal inflammation. Therefore, we aimed to investigate the role of β-estradiol and progesterone in human monocyte immune responses, at cellular and molecular levels, to identify their role as a possible immunological link between pregnancy and periodontal disease. MATERIAL AND METHODS Primary human monocytes were purified from human peripheral blood mononuclear cells by adherent method. Expression of Toll-like receptor (TLR) 2, 4 and CD14 was analyzed by flow cytometry. TLR2, TLR4, cyclooxygenase-2 (COX2), nuclear factor-kappa B (NF-κB) and NF-κB inhibitor-alpha mRNA expressions were measured using real-time reverse transcriptase-polymerase chain reaction and prostaglandin E2 secretion was assayed by enzyme-linked immunosorbent assay. NF-κB expression was also examined by immunofluorescence. Western blotting was performed to determine the activation of mitogen-activated protein kinase pathway. RESULTS We report herein that both β-estradiol and progesterone significantly reduced TLR2 expression at both protein and mRNA levels but had less of an effect on TLR4 expression in primary human monocytes. We also found that the hormones decreased monocyte cell surface protein expression of CD14. Significantly, β-estradiol and progesterone dose-dependently downregulated monocyte expression of COX2 mRNA. Pretreatment monocytes with β-estradiol or progesterone reduced effects of Porphyromonas gingivalis lipopolysaccharide (LPS) on COX2 mRNA expression and decreased prostaglandin E2 secretion by the monocytes. Furthermore, we demonstrated that both β-estradiol and progesterone inhibited P. gingivalis LPS-induced NF-κB signaling pathway through the upregulation of NF-κB inhibitor-alpha expression. However, neither β-estradiol nor progesterone altered the phosphorylation of the p38, the extracellular signal-regulated kinase 1/2 and the c-Jun N-terminal activated kinase in P. gingivalis LPS-stimulated monocytes. Thus, the inhibitory effects of these hormones on the response of human monocytes to P. gingivalis LPS appear to be independent on mitogen-activated protein kinase signaling pathway. CONCLUSION The results of the present study suggest that β-estradiol and progesterone could influence the immune response of human monocytes to periodontal pathogens and this process may have a role in the clinical manifestations of periodontal disease associated with pregnancy.
Monoclonal antibodies (MoAb) were produced against somatic antigens of adult human liver fluke Op... more Monoclonal antibodies (MoAb) were produced against somatic antigens of adult human liver fluke Opisthorchis viverrini. Earlier studies attached diagnostic potential to an 89-90 kD antigen present in both somatic extracts and in vitro culture supernatants as well as to the abundant 16-17 kD tegumental protein doublet. Mice made excellent immune responses to low dose somatic extract adsorbed onto nitrocellulose or to the 80-95 kD region of SDS gel Western blots. The antigen specificities of hybridomas reactive with somatic antigen by ELISA were determined by radioimmunoprecipitation or immunoblotting. Six MoAb reacted with the desired 16 kD tegumental protein. A 90 kD somatic protein was identified by 9 clones. By indirect immunofluorescence, monoclonals reactive with the 16 kD polypeptide identified the outermost surface of the tegument. The 90 kD antigen was associated with all major muscle systems, most strikingly the crossed subtegumental layers, oral and ventral suckers, pharynx and a thin layer surrounding caeca. The biochemical identity of this muscle-associated antigen is unknown, but it is clearly distinct from the previously identified species-specific 89 kD exoantigen. The 16 kD tegumental protein shares epitopes with a number of related flukes. However, 2 MoAb which react with this protein show no crossreaction.
Periodontitisisaninflammatorydiseaseinducedbybacterialinsultandhostimmuneresponse.�Epidemiologica... more Periodontitisisaninflammatorydiseaseinducedbybacterialinsultandhostimmuneresponse.�Epidemiological� and clinical studies over the past decade have suggested its association with development of atherogenesis, which may lead to cardiovascular disease and its complications. Lifestyle diseases are non-communicable chronic diseases of longevity that are increasing in frequency as countries become more industrialized and people live longer. The lifestyle diseases, including for example atherosclerosis, cardiovascular diseases, stroke, type 2 diabetes mellitus, obesity and osteoporosis, are at present increasing at an alarming rate worldwide, and are related largely to diet and thewayapersonlives.�Thelongofficehourandthetypeofactivitiesweencounterdailyinourofficemakeusinthe� dental professions are at risk for developing lifestyle diseases. Healthy lifestyle factors include good nutrition, regular exercise, non-smoking and body mass index of less than 25 kg/m 2 , etc. Because the oral cavit...
Beneficial effects of Va and/or Zn supplementation of children in NE Thailand are described in a ... more Beneficial effects of Va and/or Zn supplementation of children in NE Thailand are described in a companion abstract. In the same study, blastogenic response (BR) of T-lymphocytes to concanavalin-A (ConA) and PPD were assayed in cultures containing mononuclear cells (MNC) or whole blood (WB). Methods were previously described. Children were previously vaccinated with BCG. BR to ConA of MNC or
Monoclonal antibodies (MoAb) were produced against a major soluble metabolic product (excretory-s... more Monoclonal antibodies (MoAb) were produced against a major soluble metabolic product (excretory-secretory, ES) of Opisthorchis viverrini. The latter was obtained in a form of spent culture medium in which the adult flukes had been maintained in vitro. The MoAb produced were exclusively associated with either IgG or IgM isotypes. When screened against a panel of parasite antigens by indirect ELISA, these MoAb exhibited three patterns of reactivity. Approximately 50% of the MoAb were highly specific for O. viverrini and another 25% cross-reacted only with Clonorchis sinensis. The remaining 25% cross-reacted extensively with other parasites. Results from radioimmunoprecipitation and immunoblotting experiments showed all MoAb to react with the 89-kDa glycoprotein. By indirect immunofluorescence, these MoAb reacted almost exclusively with the tegumental surface, tegumental cells, cecum and developing miracidium. Different lines of evidence suggest that these MoAb reacted with different epitopes on the same 89-kDa polypeptide carrier.
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