ライフサイエンスコーパス: neurogenic inflammation

1 ensory function in neurons, causing pain and neurogenic inflammation.

2 uous airway inflammation, a process known as neurogenic inflammation.

3 n in sensory nerve endings can contribute to neurogenic inflammation.

4 s are important mediators of pain, itch, and neurogenic inflammation.

5 TRPV4 deletion attenuated PAR(2)-stimulated neurogenic inflammation.

6 d oil, demonstrating that NMB contributes to neurogenic inflammation.

7 ng increasingly blurred by new insights into neurogenic inflammation.

8 ies in primary afferents and are involved in neurogenic inflammation.

9 important role than DRRs in formalin-induced neurogenic inflammation.

10 heral chemosensory neurons, causing pain and neurogenic inflammation.

11 licated in somatosensory function, pain, and neurogenic inflammation.

12 plasma extravasation, which is a measure of neurogenic inflammation.

13 nduce a local inflammatory response known as neurogenic inflammation.

14 lows bidirectional communication, leading to neurogenic inflammation.

15 in nerves may indicate its participation in neurogenic inflammation.

16 y opposing the action of Substance P (SP) in neurogenic inflammation.

17 gered lipid mediators and may be relevant in neurogenic inflammation.

18 ther investigation in models of migraine and neurogenic inflammation.

19 nomedical use for disorders characterized by neurogenic inflammation.

20 g pain and release neuropeptides that induce neurogenic inflammation.

21 CGRP, which affect intraocular pressure and neurogenic inflammation.

22 tide (iCGRP), a neuropeptide associated with neurogenic inflammation.

23 s into infected or injured tissue, producing neurogenic inflammation.

24 bitter taste signaling in murine BCs induces neurogenic inflammation.

25 nd neuropeptide release, leading to pain and neurogenic inflammation.

26 ptide (CGRP) from sensory neurons to promote neurogenic inflammation.

27 llary permeability and blood flow to produce neurogenic inflammation(1,2), but whether nociceptors al

28 d adjacent meningeal cells and tissues cause neurogenic inflammation, a critical target for current p

29 mental evidence that P2X3 antagonism reduces neurogenic inflammation, a phenomenon hypothesised to co

30 llodynia requiring TRPM8, demonstrating that neurogenic inflammation alters cold sensitivity via loca

31 es of primary afferent neurons that initiate neurogenic inflammation and are required for the develop

32 precise mechanism underlying this so-called neurogenic inflammation and associated pain has remained

33 kinin neuropeptide, has been associated with neurogenic inflammation and asthma; therefore, we chose

34 PV1 and TRPA1 are thought to be required for neurogenic inflammation and development of inflammatory

35 erapy may include antibodies to mediators of neurogenic inflammation and even treatment of bacteria i

36 odulate neuronal IL-13Ra2, thereby promoting neurogenic inflammation and exacerbating AD and itch.

37 Capsaicin causes neurogenic inflammation and has analgesic and anti-infla

38 PAR(2)) on primary sensory neurons to induce neurogenic inflammation and hyperalgesia.

39 (PAR2) on primary afferent neurons to cause neurogenic inflammation and hyperalgesia.

40 to sickle pain pathophysiology by promoting neurogenic inflammation and nociceptor activation via th

41 l vanilloid 1 (TRPV1) channel contributes to neurogenic inflammation and pain hypersensitivity, in pa

42 ssed in primary sensory neurons that mediate neurogenic inflammation and pain transmission, and PAR(2

43 As a mediator of neurogenic inflammation and pain, we hypothesized that l

44 P) channels of nociceptive neurons to induce neurogenic inflammation and pain.

45 red ligand that excites nociceptors, causing neurogenic inflammation and pain.

46 flammatory proteases, is a major mediator of neurogenic inflammation and pain.

47 potential (TRP) ion channels, which amplify neurogenic inflammation and pain.

48 ential vanilloid 1 (TRPV1) activation causes neurogenic inflammation and plays an important role in a

49 ation elicits robust pain behaviours without neurogenic inflammation and produces profound hypersensi

50 e term toxogenetics) is sufficient to induce neurogenic inflammation and recapitulates major colonic

51 tors in airway sensory neurons, resulting in neurogenic inflammation and respiratory hypersensitivity

52 Neurogenic inflammation and the role of nerve growth fac

53 and skin barrier impairment, culminating in (neurogenic) inflammation and itch.

54 inflammatory diseases such as periodontitis, neurogenic inflammation, and inflammatory pain likely vi

55 activation may contribute to periodontitis, neurogenic inflammation, and inflammatory pain.

56 fection, wound healing, periodontal disease, neurogenic inflammation, and inflammatory pain.

57 al tumor invasion of intrapancreatic nerves, neurogenic inflammation, and tumor metastases along extr

58 Our findings suggest that a neurogenic inflammation axis ET-1/ETAR/TRPA1 contributes

59 immune-mediated skin disease associated with neurogenic inflammation, but the underlying molecular me

60 Substance P (SP), involved in neurogenic inflammation by acting through its receptor N

61 y was to determine the role of DRR and AR in neurogenic inflammation by examining the blood perfusion

62 Here we report that TcdB induces neurogenic inflammation by targeting gut-innervating aff

63 nsequently, this work provides evidence that neurogenic inflammation can be induced in the human airw

64 l pathway mediates allodynia associated with neurogenic inflammation, contributing to the algesic act

65 Our findings suggest that SP released during neurogenic inflammation enhances the responses of sensor

66 n (1% in 25 microl), which is known to cause neurogenic inflammation, failed to produce edema formati

67 cetylcholine receptors prevents SCC-mediated neurogenic inflammation for both denatonium and the bact

68 e results suggest: (1) an important role for neurogenic inflammation in pancreatitis and pain-related

69 s experimental inflammatory hyperalgesia and neurogenic inflammation in rats and naturally occurring

70 he periphery and these signals can result in neurogenic inflammation in the innervated tissue.

71 primary mediator of an axon reflex mediating neurogenic inflammation in the intestine.

72 id 1 (TRPV1) receptors in the development of neurogenic inflammation in the pelvis and pelvic organ c

73 gate whether substance P (SP) contributes to neurogenic inflammation in the skeletal muscle tissue.

74 SP does not play a critical role in inducing neurogenic inflammation in the skeletal muscle tissue.

75 tion by nociceptors which in turn constrains neurogenic inflammation in the skin.

76 f trigeminal pain fibers by capsaicin evokes neurogenic inflammation in the surrounding epithelium.

77 skin (neurogenic spots), caused by cutaneous neurogenic inflammation, in the dermatome that overlaps

78 Neurogenic inflammation is believed to originate with th

79 Significantly, TRPA1-dependent neurogenic inflammation is greater in mice anesthetized

80 These data raise the possibility that neurogenic inflammation is not a major factor in headach

81 s innervating the bladder and resulting in a neurogenic inflammation localized to the bladder.

82 tic inflammation, and a promising target for neurogenic inflammation management.

83 This new mechanism of protease-induced neurogenic inflammation may contribute to the proinflamm

84 In turn, the neuropeptides released during neurogenic inflammation may play important roles in the

85 n precipitated by stress and seem to involve neurogenic inflammation (NI) of the dura mater associate

86 ence debilitating headaches that result from neurogenic inflammation of the dura and subsequent sensi

87 flexes, including sneezing, apnea, and local neurogenic inflammation of the mucosa.

88 ere, we show that an acupoint is one form of neurogenic inflammation on the skin.

89 nal SP levels may be involved in maintaining neurogenic inflammation or the development of airway hyp

90 ETAR and TRPA1, a cation channel involved in neurogenic inflammation, pain, and itch.

91 fense, drug-induced anaphylactoid reactions, neurogenic inflammation, pain, itch, and chronic inflamm

92 oduction of Arc in afferent fibers regulates neurogenic inflammation potentially through intercellula

93 Thus, targeting neurogenic inflammation provides a host-oriented therape

94 Neurogenic inflammation quickly appeared at acupoints on

95 In MO-treated rats, acupoints showing neurogenic inflammation (termed "neurogenic spots" or Ne

96 Using the rat model of neurogenic inflammation, the albumin extravasation ratio

97 ice undergo sciatic nerve injury to activate neurogenic inflammation, they are protected from the dev

98 rigger efferent release of neuropeptides and neurogenic inflammation typically produced by noxious el

99 tor calcitonin gene-related peptide mediates neurogenic inflammation via the calcitonin receptor-like

100 d whether inflammatory mediators that induce neurogenic inflammation via the nociceptive ion channels

101 us pain, hyperalgesia/allodynia and signs of neurogenic inflammation were studied clinically and ther

102 Moreover, chronic inflammatory pain and neurogenic inflammation were unaffected by loss of the t

103 perimentally as an inducer of acute pain and neurogenic inflammation, which are largely mediated by t

104 ted peptide (CGRP) and substance P, inducing neurogenic inflammation, which further exasperates pain.

105 Neurogenic inflammation, which results from peripheral r

106 conduction of these spikes may contribute to neurogenic inflammation while orthodromic (centripetal)

107 This neurogenic inflammation within the meninges has been sug