The Costs of Living Together: Immune Responses to the Microbiota and Chronic Gut Inflammation

Abstract

While the vertebrate microbiota is critical to the normal function of many host traits, hosts may expend a large amount of energy to constrain and interface with their microbiota via their immune system to avoid the high fitness costs associated with gut dysbiosis, pathobionts, and opportunistic pathogens. All jawed vertebrates share mucosal immunity dedicated to isolating the microbiota, and a breakdown of this system can result in chronic gut inflammation. In humans, chronic gut inflammation negatively affects growth and development. There is little information available on the prevalence of chronic gut inflammation in wild animals, but given that animals with different life histories emphasize different immune responses, it follows that wild animals may vary in their susceptibility to chronic gut inflammation, and most animals will experience signaling that can lead to this state. These can be top-down signals originating from sources like the central nervous system or bottom-up signals originating from changes in the gut microbiota. The sources of these signals might include stress, developmental transitions, food restriction, and dietary shifts. Here, we briefly discuss host-microbiota interactions from the perspective of life history theory and ecoimmunology, focusing on the mucosal immune system and chronic gut inflammation. We also include future directions for research and the tools necessary to investigate them.

The microbiota influences the Drosophila melanogaster life history strategy

“…To date, research on interactions between microbiota and the life history strategy of the host has focused exclusively on how interand intraspecific variation in host life history strategies influences the microbiota (Emmett, Youngblut, Buckley, & Drinkwater, 2017;Neave et al, 2017). The reverse question-the impact of the microbiota on the life history strategy of the host-has, to our knowledge, rarely been considered (Kirschman & Milligan-Myhre, 2019;Macke, Tasiemski, Massol, Callens, & Decaestecker, 2017) and has not been investigated empirically.…”

The Impact of Rhodiola Rosea On Biomarkers of Diabetes, Inflammation, and Gut Microbiota in a Leptin Receptor-Knockout Mouse Model

“…Obesity, speci cally visceral adiposity, causes systemic in ammation through in ltration of adipose tissue by macrophages 16,17 and production of pro-in ammatory cytokines such as TNF-α, IL-1β, IL-6, and CCL2 18,19 , which act as antagonists of insulin signaling 20 . Recent studies also suggest that differences in the human gut microbiome between normal and diabetic subjects 21 are linked to systemic in ammation through altered gut integrity 22,23 , increased circulating gram-negative bacteria and endotoxin 22,24 , as well as lipopolysaccharide (LPS)-induced in ammatory cytokine secretion through TLR-4 signaling 24,25 . Evidence in humans also suggests that certain gut microbiome compositions may predispose individuals to conditions such as obesity and diabetes 26,27 .…”

“…Evidence in humans also suggests that certain gut microbiome compositions may predispose individuals to conditions such as obesity and diabetes 26,27 . As crucial components that moderate host health and physiology, the gut microbiome can contribute to in ammation, alterations of intestinal linings, dyslipidemia, and a wide variety of other changes 23 . However, studies also indicate that modulation of the gut microbiome can decrease LPS-induced systemic in ammation in a mouse T2D model, thereby counteracting these changes 25 .…”

The impact of Rhodiola rosea on biomarkers of diabetes, inflammation, and microbiota in a leptin receptor-knockout mouse model

“…Obesity, specifically visceral adiposity, causes systemic inflammation through infiltration of adipose tissue by macrophages 16 , 17 and production of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6, and CCL2 18 , 19 , which act as antagonists of insulin signaling 20 . Recent studies also suggest that differences in the human gut microbiome between normal and diabetic subjects 21 are linked to systemic inflammation through altered gut integrity 22 , 23 , increased circulating gram-negative bacteria and endotoxin 22 , 24 , as well as lipopolysaccharide (LPS)-induced inflammatory cytokine secretion through TLR-4 signaling 24 , 25 . Evidence in humans also suggests that certain gut microbiome compositions may predispose individuals to conditions such as obesity and diabetes 26 , 27 .…”