Hyaluronan: A Neuroimmune Modulator in the Microbiota-Gut Axis

The commensal microbiota plays a fundamental role in maintaining host gut homeostasis by controlling several metabolic, neuronal and immune functions. Conversely, changes in the gut microenvironment may alter the saprophytic microbial community and function, hampering the positive relationship with the host. In this bidirectional interplay between the gut microbiota and the host, hyaluronan (HA), an unbranched glycosaminoglycan component of the extracellular matrix, has a multifaceted role. HA is fundamental for bacterial metabolism and influences bacterial adhesiveness to the mucosal layer and diffusion across the epithelial barrier. In the host, HA may be produced and distributed in different cellular components within the gut microenvironment, playing a role in the modulation of immune and neuronal responses. This review covers the more recent studies highlighting the relevance of HA as a putative modulator of the communication between luminal bacteria and the host gut neuro-immune axis both in health and disease conditions, such as inflammatory bowel disease and ischemia/reperfusion injury.

AVIAN ESCHERICHIA COLI INFECTION IN MEAT-TYPE CHICKEN: PREVALENCE AND PATHOLOGY

Avian colibacillosis is considered the major bacterial disease in the poultry industry worldwide. This study was conducted to determine prevalence and pathology by avian pathogenic Escherichia coli (APEC) in broiler chicken. Various organs of affected broilers were checked for the E. coli infection. One hundred and forty commercial poultry farms were divided into seven age groups (A, B, C, D, E, F, and G). Group A (1st week), B (2nd week), C (3rd week), D (4th week), E (5th week), F (6th week), G (7th to 9th week). Investigations were conducted from day 1 until the marketing of birds based on clinical findings. A total of 2491 (23.71% of sick birds) dead birds were observed positive for E. coli infection. Three forms of infection were observed i.e. omphalitis, colisepticaemia, and colibacillosis at the rate of 1.55, 17 and 56.65%, respectively. Omphalitis was confirmed by microbial culture and revealed in only groups A and B with 76.24 and 23.76 respectively. While, Colisepticaemia was observed at the rate of 3.11, 6.74, 20.18, 29.63, 19.16, and 22.18 in groups B, C, D, E, F, and G respectively. Whereas Colibacillosis was noticed as 0.075, 3.35, 5.99, 19.20, 26.70, 16.11 and 28.55% in groups A, B, C, D, E, F, and G respectively. Petechiation of heart, kidney, and gizzard besides hemorrhagic enteritis, hemorrhagic tracheitis, and necrotic foci on the liver and caseous exudates in air sacs were the prime gross lesions noticed in colibacillosis. Microscopically, no lesion was observed in serosa, muscularis externa, and submucosa. However, loss of epithelial tissue and breaches in the mucosal layer of the small intestine were observed. Furthermore, characteristic pink and grayish colonies were observed in E. coli cultures on McConkey’s and Blood agar respectively.

Primary Site of Coxsackievirus B Replication in the Small Intestines: No Proof of Peyer’s Patches Involvement

Background: Enterovirus (EV) infections are associated with a broad range of diseases. Since the first experimental infection of primates with poliovirus (PV), tonsils and the Peyer’s patches (PPs) have been believed to be the primary replication sites of EVs. Our aim was to localize different viral markers in the small intestines (SI) of coxsackievirus B (CVB) orally and intraperitoneally (i.p.) infected mice. Methods: Transverse sections of SIs of both infected and control male outbred mice were collected at different intervals post-infection (p.i) and analyzed for presence of interferon-alpha (IFN-α) and viral protein VP1 by immunohistochemistry and in situ hybridization (ISH). Fluorescent marker, eGFP, was identified in cryosections of mice infected with eGFP-CVB3. Results: In the infected SIs, we observed enlarged germinating centers (GCs) in the PPs; IFN-α was detected in the PPs and mucosal layer of the SIs. However, VP1, viral RNA and the eGFP were absent in the GCs of PPs at all stages of infection irrespective of the virus strains used. Conclusions: Virus was present in the epithelial cells but not in GCs of the PPs of the murine SIs. Our results do not support the hypothesis of EV replication in the PP especially in the GCs.

Pathogenicity Comparison Between QX-Type And Mass-Type Infectious Bronchitis Virus To Different Segments of The Oviducts In Laying Phase

BackgroundThe QX-type infectious bronchitis virus (IBV) has become the predominant genotype worldwide in recent years and has caused serious economic losses to the chicken industry. The most significant feature of QX IBV is that its infection in the early growing stage can cause abnormal oviduct development, resulting in a high proportion of ‘false layers’ in poultry flocks of laying hens and breeders. However, few studies have evaluated whether infections of QX-type IBV in laying stages can also cause severe pathological changes in the oviduct. MethodsIn this study, 300-day-old specific-pathogen-free (SPF) chickens were infected either with the QX-type strain QXL or Massachusetts (Mass)-type strain M41 to compare their pathogenicity on different segments of the oviduct. ResultsBoth the QXL and M41 strains successfully replicated in all segments of the oviduct; however, the QXL strain was more highly distributed in mucosal layer and caused severe lesions in the lamina propria, including interstitial dilation, inflammatory cell infiltration, and distinct expansion of tubular glands. Moreover, the QXL strain induced high expression of proinflammatory cytokines and cytotoxic molecules in the majority of segments in the oviduct. Further research found that the QXL strain may affected the formation of shell membranes and eggshells by inhibiting the expression of type I collagen and CaBP-D28k. ConclusionsOur results indicate that the QX-type IBV is more pathogenic than Mass-type IBV to oviduct in laying phase. Collectively, these findings provide detailed information on the pathological changes in different segments of the oviduct in laying phase, which could offer a better understanding about the pathogenicity of IBV.

Wolf in Sheep’s Clothing: Clostridioides difficile Biofilm as a Reservoir for Recurrent Infections

The microbiota inhabiting the intestinal tract provide several critical functions to its host. Microorganisms found at the mucosal layer form organized three-dimensional structures which are considered to be biofilms. Their development and functions are influenced by host factors, host-microbe interactions, and microbe-microbe interactions. These structures can dictate the health of their host by strengthening the natural defenses of the gut epithelium or cause disease by exacerbating underlying conditions. Biofilm communities can also block the establishment of pathogens and prevent infectious diseases. Although these biofilms are important for colonization resistance, new data provide evidence that gut biofilms can act as a reservoir for pathogens such as Clostridioides difficile. In this review, we will look at the biofilms of the intestinal tract, their contribution to health and disease, and the factors influencing their formation. We will then focus on the factors contributing to biofilm formation in C. difficile, how these biofilms are formed, and their properties. In the last section, we will look at how the gut microbiota and the gut biofilm influence C. difficile biofilm formation, persistence, and transmission.

Role of Pulmonary Surfactant in Gas Exchange Mechanism and Providing Protection against Progression of any Respiratory Viral Disease like SARS-CoV-2 and Need to focus it as First Point of Medication for all Respiratory Diseases

During inhalation oxygen molecules are drawn towards type I cells. The partial pressure difference and solubility factor act as a Drive for this movement of oxygen molecules.It is well known that the pulmonary surfactant plays an important role in gas exchange. The surfactant is thin mono-layer. The top surface of surfactant with SP-B and C proteins faces alveolar air and is hydrophobic in nature and acts as a surface tension reducer, whereas lower surface with SP-A and D proteins, is hydrophilic and is adsorbed on mucosal layer. This lower surface of surfactant acts as an anti invader, pathogen barrier. However there is a small missing link in explaining its exact mechanism or role in justifying these properties during normal conditions and during ‘viral ligand’ attack.Similarly a unique physical property of SP- C component is listed in research papers; however its application is not researched anywhere. SP-C has a dielectric constant of 2 to 3 and plays a very critical role in drastically reducing progression of any respiratory viral disease including SARS-CoV-2. This hypothesis targets to explain both micro mechanisms with the help of basic laws of physics, and fluid mechanics. The figures/sketches, drawn also depict the physics involved and not much of a physiology or genetic codes etc. Two examples, in the industry, are briefly listed in the last paragraphs to draw some parallel with above mechanisms.Vaccination is a proven method for containment of a particular respiratory viral disease, if not its cure. But if focus is also given on health of pulmonary surfactant with respect to pathogenesis of any respiratory viral disease, and development of a broad spectrum medication on it; probable loss of lot many lives can be avoided and vaccine development and vaccination management related issues can be less panicky.

​The Histopathology of Alimentary Canal of Stinging Catfish Heteropneustes fossilis (Bloch, 1794), Susceptible for Trematodes Incursion

Background: Heteropneustes fossilis (Bloch, 1794) is one of the popular freshwater fish known for its food quality and nutritional value. This study was undertaken with an aim to find out histopathological changes in the intestine of freshwater fish Heteropneustes fossilis, host of trematode parasite Masenia vittatusia Agarwal, 1963. Methods: The intestine of uninfected fish used to determine normal anatomy, while infected intestine to determine pathological changes. The normal histological procedure was followed, which included fixing, rinsing, dehydrating and embedding of tissue. Tissue was cut in 4-6 µm thick sections using a rotary microtome. Haematoxylin and eosin stains were used. Result: The highest damage was observed in the mucosal layer with ruptured and fused microvilli, hyperplasia of villi, damaged columnar epithelium layer and spread of loose connective tissue into the lumen. Other degenerative modifications included hypertrophy of blood vessels in mucosa and muscularis part, some of them ruptured might be the cause of haemorrhage inside the layers. Other changes include variation in the routine shape of all three layers. The mucosal layer showed aggregation of lymphocytes and mast cells as well.

Clinical and Image Characteristics of IgG4-Related Sclerosing Cholecystitis

Since autoimmune pancreatitis (AIP) was established as a new disease entity, sclerosing change with abundant immunoglobulin-4 (IgG4)-positive plasma cells, storiform fibrosis, and obliterative phlebitis are main pathological features in IgG4-related diseases. Regarding IgG4-related sclerosing cholecystitis (IgG4-CC), which is occasionally associated with AIP cases and is rarely isolated, there are no diagnostic criteria and insufficient perceptions of the image findings. Although there have been some reports on IgG4-CC, differentiation between IgG4-CC and gallbladder cancer is very difficult in some cases with a localized lesion. In this review, we especially focused on image findings of IgG4-CC and summarized its image features for diagnostic assistance. The ultrasonography and CT findings of IgG4-CC could be classified into diffuse and localized types. Based on these findings, the presence of wall thickening with an intact or smooth mucosal layer, followed by a homogenously thickened outer layer, would be a helpful morphological finding to distinguish IgG4-CC from gallbladder cancer.

Role of Pulmonary Surfactant in Gas Exchange Mechanism and Providing Protection against Progression of any Respiratory Viral Disease like SARS-CoV-2 and Need to focus it as First Point of Medication for all Respiratory Diseases

During inhalation oxygen molecules are drawn towards type I cells. The partial pressure difference and solubility factor act as a Drive for this movement of oxygen molecules.It is well known that the pulmonary surfactant plays an important role in gas exchange. The surfactant is thin mono-layer. The top surface of surfactant with SP-B and C proteins faces alveolar air and is hydrophobic in nature and acts as a surface tension reducer, whereas lower surface with SP-A and D proteins is hydrophilic and is adsorbed on mucosal layer. This lower surface of surfactant acts as an anti invader, pathogen barrier. However there is a small missing link in explaining its exact mechanism or role in justifying these properties during normal conditions and during ‘viral ligand’ attack.Similarly a unique physical property of SP- C component is listed in research papers; however its application is not researched anywhere. SP-C has a dielectric constant of 2 to 3 and plays a very critical role in drastically reducing progression of any respiratory viral disease including SARS-CoV-2. This hypothesis targets to explain both micro mechanisms with the help of basic laws of physics, and fluid mechanics. The figures/sketches, drawn also depict the physics involved and not much of a physiology or genetic codes etc. Two examples, in the industry, are briefly listed in the last paragraphs to draw some parallel with above mechanisms.Vaccination is a proven method for containment of respiratory viral disease, if not its cure. But if focus is also given on health of pulmonary surfactant with respect to pathogenesis of any respiratory viral disease, probable loss of lot many lives can be avoided and vaccine development and vaccination management related issues can be less panicky.

Dysbiosis of Fecal Microbiota From Complement 3 Knockout Mice With Constipation Phenotypes Contributes to Development of Defecation Delay

Significant phenotypes for constipation were detected in complement 3 (C3) knockout (KO) mice, although no research has been conducted on an association with alteration of gut microbiota. To investigate the effects of dysbiosis on fecal microbiota from C3 KO mice with constipation, the composition of fecal microbiota was characterized in mid-colons of 16-week-old C3 KO mice, and their function for defecation delay development was examined after fecal microbiota transplantation (FMT) of C3 KO mice. Some significant alterations in constipation phenotypes, including stool parameters and histopathological structure, were detected in 16-week-old C3 KO mice compared to those of wild-type (WT) mice. Fecal microbiota of C3 KO mice exhibited decreases in Anaerocolumna, Caecibacterium, Christensenella, Kineothrix, and Oscillibacter populations and increases in Prevotellamassilia, Reuthenibacterium, Prevotella, Eubacterium, Culturomica, Bacteroides, and Muribaculum populations. In FMT study, key stool parameters, including weight and water content, were remarkably declined in a transplanted KO (KFMT) group of antibiotics-induced depletion of microbiota (AiDM)-WT and AiDM-KO mice, and a similar change was observed in fecal morphology. However, intestine length decreased in only the KFMT group of AiDM-WT mice compared with that of AiDM-KO mice. The mucosal layer and muscle thickness were commonly decreased in the KFMT group of AiDM-WT and AiDM-KO mice, and significant alterations in the crypt structure of Lieberkuhn and molecular regulators, including AQP8, C-kit, and 5-HT, were observed in the same group. Taken together, results of the present study indicate that dysbiosis of fecal microbiota from C3 KO mice with constipation phenotypes has a key role in the induction and regulation of defecation delay.