Mechanisms of immune resolution

Abstract

Initially after injury, the innate/proinflammatory and some aspects of the acquired immune response are up-regulated to maintain a defense against foreign pathogens, clear tissue debris present at the wound site, and orchestrate aspects of tissue remodeling, cell proliferation and angiogenic process, associated with the wound response. However, for proper wound healing to progress, this initial inflammatory response has to be regulated or shut down so as to allow for the reestablishment of matrix, recellularization, and tissue remodeling. Inability to properly resolve the extent of innate/ acquired response at a site of injury can lead to poor wound healing, immune suppression, and recurrent infectious episodes. This review attempts to summarize information on regulatory mechanisms that are thought to be involved in controlling/resolving innate or acquired immune responses so as to provide a framework for use in thinking about the impact these processes and their manipulation may have on wound healing and its potential management.

In Vitro Cow's Milk Protein-Specific Inflammatory and Regulatory Cytokine Responses in Preterm Infants With Necrotizing Enterocolitis and Sepsis

“…Animal studies have shown that septic mice with TGF-␤1 gene deletions develop spontaneous organ failure associated with infiltration of MNCs, which indicates that this gene may play a role in controlling inflammatory responses (16). In addition to its immunologic effects, TGF-␤1 is also known for its enhancing effect on fibrous tissue formation (17).…”

NFκB Is Persistently Activated in Continuously Stimulated Human Neutrophils

“…In addition to their phagocytic and killing properties, neutrophils synthesize numerous proinflammatory cytokines and chemokines that may amplify the inflammatory process (5)(6)(7)(8)(9). Furthermore, recent studies have shown that neutrophil apoptosis is delayed in patients with sepsis, ALI, and BPD (10)(11)(12). Expression of many of these proinflammatory and antiapoptotic genes is regulated at the level of transcription by the transcription factor NFκB (13)(14)(15)(16)(17)(18)(19)(20)(21)(22).…”

Accumulation of DC in Lamina Propria Induced by FMS-Like Tyrosine Kinase 3 Ligand Aggravates the Intestinal Inflammatory Response During Endotoxemia

“…Following the recognition of a pathogen, APC and lymphocytes are activated leading to the production of pro-inflammatory cytokines, processes that are tightly controlled as a local inflammatory process under normal circumstances. Uncontrolled or amplified inflammation can lead to septic shock and damage to host tissue [38]. In the steady state DC in the intestine, under the conditioning of intestinal epithelium, predominantly induce TH2-type response to avoid pathological inflammatory response.…”