Microbiota Immune System

The relationship between the human gut microbiome to health and disease is strong. Human physiology, metabolism, nutrition, and immune function are all affected by the composition of the gut. If the composition of the gut microbiome is altered in a way that any of these functions are negatively affected, this can lead to disease. The developments of the microbiome, its complexity, and its functionality in health and disease have been extensively studied. In addition, the way in which it is altered has many implications in the cause of diseases, such as bowel disease, obesity, diabetes and cancer.

The effect of different diets on the gut microbiome has been studied greatly in mice and to a lesser extent in humans to assess the effect that dietary composition has on the gut micro-biome. It has been suggested that increased efficiency of energy harvest due to changes in the gut microbiota with an increase in Firmicutes and decrease Bacteroidetes bacteria, occurs in obesity in mice and humans.4 A study performed by Murphy et al looked at the effect of a high-fat (HF) diet and genetic obesity (ob/ob) for changes in gut microbiota and the amount of energy harvested from food over time.4 Ob/ob mice were fed a low-fat diet and wild-type mice were fed either a low-fat or HF-diet for 8 weeks. Results indicated an increase in Firmicutes bacteria in both mice fed a HF diet as well as ob/ob mice, but Firmicutes bacteria did not change over time in the lean control mice. A reduction in Bacteroidetes bacteria was also found in ob/ob mice.4

The good gut microbes are a powerful line of defense against pathogens and germs and also prevent the overgrowth of harmful microbes such as bacteria, yeasts and parasites, making healthy bacteria vital for a strong immune system.

Gut microbiome is one of the densest, most dynamic, and complex microorganism populations located in the body (Costa et al., 2012). Gut microbes act against transient pathogens, aid in digestion and absorption, stimulate the immune system, and support enteroctyes (Suchodoiski et al., 2012). Gut microbiome population differs between species, individuals, and organs (Fraga et al., 2011). It is noted that there are one billion microbes from one drop of cecal fluid, consisting of anaerobic microorganisms such as bacteria, fungi, protozoa, and archae (Fraga et al., 2012). If these microbes are changed, this could result in gastrointestinal disease and even death. Clostridium perfringens, Clostridium difficle, Escherichia coli general and K-12, and Streptococcus bovis/equinus complex (SBEC) are common bacteria found in the microbiome of the hindgut. These strains are considered opportunistic bacteria, and if the immune system becomes compromised by changes to the hindgut microbiome, this will trigger proliferation of harmful and opportunistic bacteria that can cause numerous gastrointestinal

Since a large portion of your immune system resides in your gut, keeping it healthy can protect you against a variety of conditions. Support your gastrointestinal health by ensuring your gut microbiome has a healthy balance of bacteria. When your gut flora is healthy, your body can perform essential functions more effectively and defend itself against harmful invaders, such as carcinogens or the flu virus. Eat more of these 10 foods for gut health and keep your gut healthy and happy.

Recent studies conducted with mice have shown that microbes in he stomach keep the immune system in check. If no microbes are detected, the immune system is weakened, increasing the risk of ailments. Rather than run from germs, society should embrace germs, as they are critical in the sustainability of our immune system.

Dr. Jeffrey I. Gordon is a researcher that works out of his lab at Washington University in St. Louis called the Centre for Genome Sciences and Systems Biology and investigates with mice and germs (The Gordon Lab, 2014). He has received many degrees such as his medical doctorate degree and many different prizes for his works in medicine (The Gordon Lab, 2014). He has many different honours from the Washington University and St. Louis University (The Gordon Lab, 2014). Gordon has conducted numerous experiments that include his 478 peer-reviewed publications and numerous collaborations with other researchers and scientists (The Gordon Lab, 2014). Gordon’s major contributions to the scientific community are very useful as much of what is known today about the stomach micro biome is mostly from Dr. Gordon’s experiments (Washington University, 2014). Dr. Gordon is also honoured and praised for his discovery that links nutritional health to the inner working of tens of trillions of microbes residing within the gut (Washington University, 2014). In one of Gordon’s peer reviewed publications called Molecular Analysis of Commensal Host-microbial Relationships in the Intestine, Gordon investigates how little microbes can adapt and shape out physiology. Gordon implanted human microbes from the gut into mice and observed the results (Gordon et al., 2005). He discovered that the microbes modulated the genes and the mice had developed many

1) [4-6, 2, 7]. Maintaining a delicate balance between tolerance and responsiveness in the intestinal mucosal immune system is very important and disruption of this balance leads to chronic intestinal inflammation [53, 4]. A properly functioning mucosal immune system, the mucosal barrier, and the presence of endogenous microbiota are the main elements in the maintenance of intestinal homeostasis [54]. The occurrence of an aberrant immune response to endogenous microbiota has been proposed to play an important role in the disease pathogenesis of CE in dogs [8, 2, 7]. Thus, phagocyte activation and their biomarkers may represent potential and useful markers of inflammation in dogs with

The average small-intestine:colon length ratio is 2.5 (Treuting and Dintzis, 2012), and the surface ratio of small intestine:colon is 18 (Casteleyn et al., 2010). The intestine of a normal conventional mouse harbours billions of commensal bacteria that are attached in the lumen and mucus protecting the underlying epithelium. (Johansson, 2015) The mucus layer of the large intestine serves as a barrier between bacteria and the mucosa which is organized in two layers, an inner, sterile mucus layer that is firmly attached to the epithelial cells and an outer, non-attached layer that forms a natural habitat for indigenous intestinal bacteria. (Johansson, 2010; Li, 2015; Pelaseyed, 2015) However, the structure of mucus differs between the small and large intestine depending on the composition of microbiota in each region. (Johansson, 2015) Mucus is made up of glycoprotein that is produced by intestinal goblet cells (Deplancke 2001). In conventional mice, these cells are mostly abundant in the proximal colon, which gradually decrease in number in the distal colon and rectum. (Nguyen, 2015) In GF mice, it has been reported that there are fewer and smaller goblet cells in

Mucosal surfaces are the main route of entry for pathogens in all living organisms. In the case of teleost fish, mucosal surfaces cover the vast majority of the animal. As these surfaces are in constant contact with the environment, fish are perpetually exposed to a vast number of pathogens. Despite the potential prevalence and variety of pathogens, mucosal surfaces are primarily populated by commensal non-pathogenic bacteria. Indeed, a fine balance between these two populations of microorganisms is crucial for animal survival. This equilibrium, controlled by the mucosal immune system, maintains homeostasis at mucosal tissues. Teleost fish possess a diffuse mucosal-associated immune system in the intestine, with B cells being one of the main responders. Immunoglobulins produced by these lymphocytes are a critical line of defense against pathogens and also prevent the entrance of commensal bacteria into the epithelium. In this review we will summarize recent literature regarding the role of B lymphocytes and immunoglobulins in gut immunity in teleost fish, with specific focus on immunoglobulin isotypes and the microorganisms, pathogenic and non-pathogenic, that interact with the immune system.

Toll-like receptors (TLRs) constitute very important players in this microbiome balance. TLRs are trans membrane non-catalytic receptor proteins that prompt activation of innate and adaptive immune responses to microorganisms through recognition of conserved molecular patterns of organisms. In order to maintain immune tolerance to the luminal microorganisms the expression of TLRs by intestinal epithelial cells is normallyat its minimal.

The immune system treats good bacterias, foods, and other valuable substances as unwanted foreign invaders, so it attacks them. As it does this, white blood cells begin to build up in the lining of the gut, which causes inflammation.

The immune system is a complex network of innate and adaptive compartments that work together in order to protect and fight against pathogenic invaders. The immune system also acts as a regulator of host homeostasis in order to ensure that the body is operating under optimal conditions. The composition of microbiota is associated with the adaptive and innate immune systems, which work together in order to maintain a constant relationship between the increasingly different microbiota and pathogens found within our body.

One of the cardinal features of mucosal immunity in mammals is the synthesis and transepithelial transport of large amounts of SIgA that contribute to maintaining homeostasis with the enteric microbiota (Macpherson et al., 2008; Mestecky, 1987). Endogenous SIgA production normally begins shortly after weaning, coincident with a shift from breast milk to solid food as the main nutrition source and accelerated colonization of the intestine by commensal bacteria. The initial endogenous SIgA response is dominated by IgA antibodies with few if any mutations in their variable regions and low avidity for the bacteria in the lumen (Lindner et al., 2012). As the mucosal immune system matures, most of the SIgA antibodies secreted in the intestine carry mutations concentrated in the complementarity-determining regions of VH and VL domains. These mutations occur as a result of T-cell dependent somatic mutation in GCs and lead to increased avidity of the antibodies for target antigens. B cell clones responding to foreign antigens that persist can undergo additional rounds of somatic mutation in GALT GCs contributing to further increases in antibody affinity (Bergqvist et al., 2013).

The human immune system has advanced to distinguish between and eliminate disease-causing microorganisms. Nevertheless, a symbiotic relationship has been developed with several species of bacteria that not only inhabit the gut, but also make up the natural commensal flora or microbiota. The microbiota, being essential in the breakdown of nutrients, helps prevent colonization by potentially pathogenic bacteria. Also, the gut commensal bacteria appear to be vital in the growth of an efficiently functioning immune system. Many studies have been done to demonstrate that various species of microbiota can cause responses from different types of immune cells such as Th17 cells and Foxp3+ regulatory T cells, suggesting that the properties of the microbiota can have a significant influence on immune response. Although the microbiota is found in the gut, it seems to have a substantial effect on immune response. In fact, specific gut commensal bacteria have displayed a correlation in affecting disease development in other organs besides the gut, and depending on the type of species, can have a wide range of effects on disease, whether that being inhibition or protection. It has also been determined that the initial composition of the microbiota is significant through the effects of milk attained by either breastfeeding or formula feeding. All in all, the gut microbiota has been found to be significant in the development of the host’s immunity to various pathogenic microorganisms, and