Enteropathy

In this article it is proposed that celiac disease be viewed not as a rare “genetically-determined” disorder, but as an extreme example of our body communicating to us a once universal, species-specific affliction: severe intolerance to wheat. Celiac disease reflects back to us how profoundly our diet has diverged from what was, until only recently a grain free diet, and even more recently, a wheat free one. We are so profoundly distanced from that dramatic Neolithic transition in cultural time that “missing is any sense that anything is missing.” The body, on the other hand, cannot help but remember a time when cereal grains were alien to the diet, because in biological time it was only moments ago.

The incidence of Antimicrobial Resistance (AMR) has been growing globally, posing threat to medical practice. Around
this instance, environmental enteropathy remains one of the major causes of infant mortality. In the past few decades,
great efforts have been laid to foster gut health. Efforts have been focused on understanding the role of exogenous factors
such as sanitation, exclusive breast feeding, consumption of probiotic nutrition, etc. Antibiotics, while treating the disease
successfully, diminishes the gut micro biome and possess the threat of developing resistance. A complementary way of
enhance gut health is to build a healthy gut micro biome environment which requires a great insight in understanding the host-microbiome interactions. Precise engineering of bacteriophages to develop novel models to understand, describe, probe and modify gut function by building a healthy micro biome environment will yield decade’s worth progress in the field of biotechnology. The objective of this article is to introduce the hypothesis of tuning gut microbiota using bacteriophages and to familiarize the physiology of a bacteriophage, to elaborate its current implications, challenges faced on its application, future scope and to motivate new researchers to bring out novel strategies to mitigate the burden and spread of Environmental Enteric Dysfunction (EED) by establishing a healthy micro biome using bacteriophage- mediated micro biome engineering which proves complementary to nutritional and chemotherapeutic approaches.
Keywords: Bacteriophage; Environmental; Enteropathy; Gut Health; Gut Micro Biome.
List of Abbreviations: AMR - Antimicrobial resistance; WHO- World Health Organisation; EED- Environmental
Enteric Dysfunction; DNA- Deoxyribo Nucleic Acid; dsDNA- Double stranded Deoxyribo Nucleic Acid; ssDNA- Single
stranded Deoxyribo Nucleic Acid; ssRNA- Single stranded Ribo Nucleic Acid; CRISPR- Clustered, Regularly Interspaced
Short Palindromic Repeats; CAS- CRISPR Associated Sequences; SiRNA- Silencing RNA; HMC- Hydroxy Methyl Cytosine
PCR- Polymerase Chain Reaction.

Background: Non-celiac gluten sensitivity (NCGS) is a syndrome that is related to the ingestion of gluten-containing food. In the current study we developed and validated a NCGS rat model.
Materials and Methods: Wistar rats were divided into 2 groups: control group (receiving 0.02 M acetic acid solution) and gliadin group (receiving 1.5 mg/g of body weight of gliadin in acetic acid solution). Rats received its treatment by intra-gastric gavage on postnatal day 2, then three times a week for 6 weeks. Animals were assessed for weight changes, intestinal permeability, histology, inflammatory cytokines, and anti-gliadin antibodies (AGA). Intestinal permeability was evaluated 24 h prior to sacrifice by administering a lactulose/mannitol solution (500/250 mg/kg respectively), and collecting urine for 24 h. For histological examination, small intestines were collected, fixed, and stained with hematoxylin and eosin. Intestinal gene expression of cytochrome P450 (CYP 3a62, CYP 3a9/18) and uptake transporters, breast cancer resistance protein (ABCG2), and P-glycoprotein (MDR1a) were evaluated using qRT-PCR. Blood was collected for measurement of totalanti-gliadin antibodies (AGA), anti-gliadin immunoglobulins A and M (AGA-IgA and AGA-IgM), and pro-inflammatory cytokines.
Results: As compared to control, the gliadin group had lower body weight, increased intestinal permeability (p<0.05); mild villous atrophy, increased intraepithelial lymphocytes, mild inflammation; increases in total AGA and AGA-IgM, increased gene expression of pro-inflammatory cytokines, IL-6, TNF-α, and IFN-γ, by 94%, 33%, and 46% (p < 0.05) and altered gene expressions of CYP450 and transporters.
Conclusions: This model closely mimics the pathological and inflammatory characteristics of NCGS, and could be used to test new pharmacological treatments for this syndrome.

Aims—To compare jejunal mucosal morphometry in HIV infected patients resident in London and Uganda.Patients—Twenty HIV positive patients from London and 16 from Uganda were studied, and compared with HIV negative control subjects from both sites.Methods—Stools and biopsy specimens were examined for enteropathogens. Surface area to volume (S:V) ratio was estimated morphometrically, mean crypt length of jejunal biopsy specimens was measured, and HIV infected cells detected immunohistochemically were quantified.Results—Enteric pathogens were detected in none of the London patients, and in three Ugandan patients. S:V ratio was lower, and mean crypt length higher, in the specimens of London patients than in normal subjects, but there was no difference in S:V ratio or mean crypt length between Ugandan patients and controls. A negative correlation was present between S:V ratio and mean crypt length in all biopsy specimens analysed. HIV infected cells were detected only in lamina propria.Co...