The innate immune response is highly dependent on the action of macrophages. They are abundant in the intestine subepithelial lamina propria of the mucosa, where they deploy multiple tasks and play a critical role. The balance between the gut microbiota and M2 macrophages is critical for gut health and homeostasis. Gut microbiota has the power to change macrophage phenotype and replenish the resident macrophage niche during and post infection. As far as the extracellular enteric parasitic infections invasive amebic colitis and giardiasis are concerned, a change of macrophages phenotype to a pro-inflammatory state is dependent on direct contact of the protozoan parasites with host cells. Macrophages induce strong pro-inflammatory response by inflammasome activation and secretion of interleukin IL-1β. Inflammasomes play a key role in the response to cellular stress and microbe attacks. The balance between gut mucosal homeostasis and infection is dependent on the crosstalk between microbiota and resident macrophages. Parasitic infections involve NLRP1 and NLRP3 inflammasome activation. For Entamoeba histolytica and Giardia duodenalis infections, inflammasome NLRP3 activation is crucial to promote the host defenses. More studies are needed to further elucidate possible therapeutic and protective strategies against these protozoan enteric parasites’ invasive infections in humans.
Abdominal wall hernias represent a clinical spectrum ranging from a small defect in the abdominal wall causing minimal interruption to patients up to massive defects with severe impairment in abdominal wall function and physiology. Principles of successful hernia repair rely on re-approximation of fascial defect edges to achieve primary closure in a tension free manner and subsequent reenforcement of the repair with a mesh. In the case of large defects, especially in the incisional hernia scenario, advanced fascial release techniques with separation of components is often required to recreate normal anatomy. Relevant techniques are anterior component separation with or without sparing of periumbilical vascular perforators and posterior component separation with transverse abdominis release, representing an expansion of the retrorectus Rives-Stoppa repair. With regards to surgical planning, preoperative imaging, standardization of techniques according to patient and hernia defect characteristics as well as prehabilitation of the abdominal wall with botulinum toxin (chemical component separation) represent significant weapons in the armamentarium of the complex abdominal wall reconstruction surgeon. The scope of this chapter is to attempt to unify pathophysiologic concepts of hernias with anatomic-based advanced repairs.