Zharp2-1

Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.

Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.

TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.

Zymosan-induced peritonitis is a sterile acute-inflammation model produced by intraperitoneal injection of zymosan, a yeast cell-wall particle preparation, followed by quantification of leukocyte recruitment and soluble inflammatory mediators in peritoneal lavage fluid. Low-dose zymosan peritonitis is commonly used as a self-resolving acute inflammation model in which neutrophil recruitment occurs early and monocyte/macrophage accumulation follows later. The assay readouts include total peritoneal leukocyte number, differential neutrophil and monocyte/macrophage counts, peritoneal cytokines and chemokines, plasma or peritoneal exudation, and optional lipidomic or metabolomic changes during inflammation and resolution. Early neutrophil recruitment after zymosan depends strongly on complement and mast-cell C5a receptor signaling, whereas later monocyte recruitment is linked to MCP-1/CCL2 production.