title: Lipopolysaccharide IP-PA1 from Pantoea agglomerans prevents suppression of macrophage function in stress-induced diseases.
abstract: Chronic psychological stress impairs health and induces various diseases by causing an imbalance in the immune, neuropsychiatric and endocrine systems. The primary reason for the development of stress-induced disease is suppression of macrophage function, which plays a pivotal role in innate immunity. In fact, surgical stress has been shown to exacerbate opportunistic infections by significantly suppressing macrophage function. Conversely, administration of macrophage activating substances before surgery, such as tumor necrosis factor (TNF)-α or Picibanil (OK-432), has been shown to protect against macrophage suppression and the resulting exacerbation of infectious diseases, and against tumor metastasis in the lungs. Thus, if suppression of macrophage function by stress could be safely prevented by use of a macrophage activating substance, the detrimental side effects of stress could be reduced. Recently, we identified a lipopolysaccharide, IP-PA1, derived from Pantoea agglomerans, a symbiotic Gram-negative bacteria found in wheat and other food plants. Oral administration of IP-PA1 demonstrated macrophage activation (priming) and protective effects against infection, allergy and cancer, without any side-effects. In this review, the possibility of using IP-PA1 as a safe, macrophage activating substance for prevention of stress-induced impairments is discussed.
authors.affiliation: Department of Nutritional Science, Okayama Prefectural University, Kuboki, Soja, Okayama 719-1197, Japan. nakata@fhw.oka-pu.ac.jp
authors.forename: Kazue
authors.initials: K
authors.lastname: Nakata
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Inagawa
authors.forename: Gen-Ichiro
authors.initials: G
authors.lastname: Soma
mesh_terms: D000284:Administration, Oral; D018712:Analgesics, Non-Narcotic / Q000008:administration & dosage / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002113:Calcification, Physiologic / Q000187:drug effects; D003907:Dexamethasone / Q000633:toxicity; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000276:immunology; D004353:Drug Evaluation, Preclinical; D005516:Food Microbiology; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D008262:Macrophage Activation / Q000187:drug effects* / Q000502:physiology; D051379:Mice; D016688:Mice, Inbred NOD; D009369:Neoplasms / Q000209:etiology / Q000517:prevention & control; D009490:Neurosecretory Systems / Q000187:drug effects; D020636:Pantoea / Q000737:chemistry*; D010945:Plants, Edible / Q000382:microbiology; D013315:Stress, Psychological / Q000150:complications / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology
chemical_list: D018712:Analgesics, Non-Narcotic; D008070:Lipopolysaccharides; C524847:lipopolysaccharide IP-PA1, Pantoea agglomerans; D003907:Dexamethasone; D006854:Hydrocortisone