|
The Journal of the Japanese Society for Clinical Microbiology |
Biblioraphy Information
ArticleTitle |
Insights into innate inflammatory responses, infectious immunity, and pathobionts |
Language |
J |
AuthorList |
Natsuo Yamamoto, Kiwamu Nakamura, Keiji Kanemitsu |
Affiliation |
Department of Infection Control, Fukushima Medical University |
Publication |
J.J.C.M.: 26 (3), 209-222, 2016 |
Received |
May 9, 2016 |
Accepted |
|
Abstract |
Recent understandings of innate inflammatory responses are summarized from the two viewpoints of "inflammasome" and "contact hyper sensitivity (CS)". Features common to the two concepts are 1. A few small molecules may initiate local, or in a severe case, to systemic host inflammatory responses in a short period of time, 2. To involve several innate immune cells, IL-1β secretion is crucial to febrile clinical symptoms, and 3. Several microbial components, pathogen associated molecular patterns (PAMPS), as well as danger signals of host elements may trigger them. Both systems are highly involved to our commonly encountered clinical febrile manifestations that include infectious, traumatic, autoimmune, drug-induced, cancer, and febrile neutropenic disorders. Invasion of host mucosal or skin barriers by foreign bacterial and intracellular, viral pathogens, or aseptic tissue damages caused by trauma, burn, hypoxic organ failure, both induce NLRs family activation, that followed by caspase-1 and IL-1β augmentations. CS also requires NALP3 and ASC components in its sensitization phase, then IL-1β secretion for its elicitation phase.
Finally, we clarified that bacterial pneumonia initiates CS-like rapid host responses via an appropriate B1a cell-derived early-acquired IgM antibody, which is also critical for CS with activation-induced cytidine deaminase (AID) assistance.
Inflammasome may be more introduced in broad clinical field since, for instance, anti-IL-1β treatment has now become available. In the same time, from the standpoint of an infection controller, broad antibiotics consumptions, several anti-inflammatory therapies, and immunomodulatory agents, run the risk of breaking the balance between host and microorganisms interactions.
Current antimicrobial stewardships would become more important to maintain individual microbiota and restrict local to global transmissions not to manifest "pathobionts" worldwide population under already-prevailed risk of drug-resistant microbes that become commensalities in healthcare associated hygiene. The importance of recognizing concept for innate inflammation and pathobionts are to be more illuminated because both systems need more sophisticated balance, and organized for global health. |
Keywords |
contact hypersensitivity, pathobionts, ONE HEALTH |
|