With constant mucus flow, changing nutrient availability, and other ecosystem stressors, our internal bionts have to quickly respond to constant flux. Microbes thrive in the gut in part because they are communal organisms. In the initial colonization of the intestines, intrepid microbes looked out on the turbulent yet nutrient-rich landscape and declared it good.  They then began the process of colonization which entailed finding an unoccupied ecological niche in the gut and massively reproducing to form dense communities. Microbes find safety in numbers, transforming the gut into an urban space. As we touched on in the previous section, bacterial species band together, forming complex networks of biofilms that allow sometimes multiple species of bacteria to cohabitate happily. Biofilms operate as packed high-rises in a congested urban environment, providing avenues for wastes, nutrients, and signals to travel so that even the most interior bacterium is cared for. Once considered solely the mark of pathogenic bacterial populations, biofilms are proving to be a valuable aspect of commensal bacteria’s ability to survive and thrive in hostile or fluctuating environments.  In order to create a biofilm, bacteria secrete various substances that allow them to form cocoon-like structures around the bacterial community.  The formation of these structures is part of the first requirement of skills for settlement in the gut. Safely ensconced in their living towers, bacteria can concentrate their abilities on extracting nutrients, the second settlement requirement, and combating adverse forces, the third. Bacteria in a biofilm can specialize because the surrounding cells are doing other specialized jobs that provide for the whole community. Structurally, biofilms anchor bacteria firmly to the mucus layer despite the surge and flow of intestinal contents, allowing molecules made by resident bacteria to pass through the colony and eventually through the mucus to our epithelial cells. It is telling that many of the microbes isolated from our guts now lack the genes for motility that are present in the genomes of their free-moving brethren.

Biofilms protect against antimicrobial agents (such as antibiotics), and make it virtually impossible for any harmful bacterial species to infiltrate and conquer the colony’s niche.  These complex colonies afford microbes protection from fierce predators: our immune cells as well as marauding viruses.  Since the bacterial colony stays in the outer edges of the mucus layer in a fairly self-contained community, it becomes less likely that any harmful organisms, substances, or human cellular police will come into direct contact with any bacterial elements.

A solitary, roving bacterium will quickly be identified as “non-self” by a patrolling macrophage, dendrite, or even the placid barrier epithelial cells. Receptors on human cells’ surfaces called pattern recognition receptors (PRR)—of which toll-like receptors (TLR) are a subset—can bind and identify certain microbial-associated molecular patterns (MAMPs) associated with microbes. To visualize this concept, think of each PRR and TLR with a pocket that is cut like a puzzle piece.  Only a puzzle piece with the complementary shape can fit into the pocket, so each MAMP has a PRR that matches its shape.  Once the non-self alarm sounds, the innate immune system moves into action, sending out defensive cells, such as the ominously named natural killer cells, whose specialties (as their name suggests) are in taking out foreign invaders.  Bacteria in biofilms are less likely to trigger the non-self alarm.

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