The roles of autotaxin/lysophosphatidic acid in immune regulation and asthma

Lysophospholipids in Lung Inflammatory Diseases

“…LPA treatment increased decoy receptors of Th2 type cytokine, such as IL-13Ra2 and soluble ST2 (sST2) [130], suggesting that LPA may attenuate IL-13-and IL-33-mediated signaling in bronchial epithelial cells, further suggesting an anti-Th2 response property of LPA in bronchial epithelial cells. As discussed by Kim S et al, these in vitro studies used LPA18:1, which is not the major LPA species in asthmatic patients (reviewed in [131]). The major species, LPA22:5 and 22:6, should be used to test and evaluate their effects on IL-13-and IL-33-mediated signaling in airway epithelial cells.…”

PKCε stimulation of TRPV1 orchestrates carotid body responses to asthmakines

“…During the early phase (occurring within 15 min and lasting 1-2 h), inflammatory mediators produced by the lungs increase (Weersink et al 1994). These asthmakines -predominantly lysophosphatidic acid (LPA) and asthma-associated prototypical Th2 cytokines including IL4, IL5, IL13 and CCL11 (eotaxin) (Kim et al 2020) -likely contribute to the late-phase asthmatic response in which airways are invaded by granulocytes and lymphocytes (Toward & Broadley, 2004;Nabe et al 2005;Gauvreau et al 2015). The mechanisms causing the early-and late-asthmatic responses are likely multifaceted involving interaction between pulmonary immune cells and parasympathetic (vagal efferent) innervation as described above (Talbot et al 2015;Drake et al 2018).…”

“…These asthmakines – predominantly lysophosphatidic acid (LPA) and asthma‐associated prototypical Th2 cytokines including IL4, IL5, IL13 and CCL11 (eotaxin) (Kim et al . 2020) – likely contribute to the late‐phase asthmatic response in which airways are invaded by granulocytes and lymphocytes (Toward & Broadley, 2004; Nabe et al . 2005; Gauvreau et al .…”

A Novel Therapeutic Reagent, KA-1002 for Alleviating Lysophosphatidic Acid-Mediated Inflammation Related Gene Expression in Swine Macrophages

“…For those various inflammatory diseases, endogenous factors associated with those environmental stresses are also important and those inflammatory endogenous factors often weaken immunity of animals leading to susceptibility to pathogenic invasion. Among various endogenous stress-induced molecules, lysophosphatidic acid (LPA) is a powerful endogenous trigger of inflammation in a number of diseases-associated conditions [7][8][9][10]. Thus, various environmental stresses induced upregulated LPA potently triggers multiple inflammatory diseases [8,10].…”

“…Among various endogenous stress-induced molecules, lysophosphatidic acid (LPA) is a powerful endogenous trigger of inflammation in a number of diseases-associated conditions [7][8][9][10]. Thus, various environmental stresses induced upregulated LPA potently triggers multiple inflammatory diseases [8,10]. LPA signaling is mediated by its receptors, LPARs and there are needs for LPA antagonists for therapeutic reagents [11,12].…”