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1 airway defense against inhaled pathogens and irritants.
2 rs chronically exposed to moderate levels of irritants.
3 after chronic exposure to moderate levels of irritants.
4 ons or exposure to allergic and non-allergic irritants.
5 hagous fluids, environmental xenobiotics and irritants.
6 ent of TRPA1, a key sensor for environmental irritants.
7 matory responses to cutaneous and peritoneal irritants.
8 y airway exposures to allergens and chemical irritants.
9 ell as environmental and endogenous chemical irritants.
10 in increased penetrability to allergens and irritants.
11 pungent natural compounds and environmental irritants.
12 y for behavioral responses to these chemical irritants.
13 nd mediates behavioral responses to chemical irritants.
14 pungent natural compounds, and environmental irritants.
15 ion of nociceptors by endogenous and natural irritants.
16 mach less susceptible to damage from luminal irritants.
17 lvents, welding fumes, and other respiratory irritants.
18 xposure to allergens, pathogens, or chemical irritants.
19 hich respond to numerous odorants as well as irritants.
20 tinocytes treated with certain allergens and irritants.
21 es to protect the host against pathogens and irritants.
22 oxyethylene) ammonium chloride (ITDOP); mild irritants: 5% 3-decyloxypropyl-bis(polyoxyethylene) amin
24 o enhance permeability and susceptibility to irritants; accordingly, increased attention should be gi
25 rritation response in mice elicited by smoke irritants (acrolein, acetic acid, and cyclohexanone).
26 ral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many diffe
27 rosols with increasing doses of the chemical irritants allyl isothiocyanate (AITC; also known as must
29 s can affect airway inflammatory response to irritants and allergens, but the importance of stress in
31 uction machinery through which environmental irritants and endogenous proalgesic agents depolarize no
33 cautions should be taken against respiratory irritants and molds and to prevent children from becomin
35 tion following long-term exposure to harmful irritants and pollutants, particularly in the airways.
36 el is the molecular target for environmental irritants and pungent chemicals, such as cinnamaldehyde
39 PCR analyses of multiple chemical allergens, irritants, and non-sensitizers have identified 10 genes
40 multiple symptomatic high-level exposures to irritants; and (iii) possible IIA, that is asthma occurr
42 ctivated by noxious heat, acid, and alkaloid irritants as well as several endogenous ligands and is s
44 side' world from potentially harmful toxins, irritants, bacteria and other pathogens that also exist
45 gions in the mouth are uniquely sensitive to irritants because they can penetrate through the tissue
46 s sensory detection of pathogens, toxins and irritants; breakdown of the epithelial barrier is associ
47 ubstances, toxins, venoms, and environmental irritants but that also trigger exuberant allergic react
50 rs after treatment, mild and moderate ocular irritants caused a significant increase in corneal thick
51 he epithelium, whereas the mild and moderate irritants caused complete epithelial cell loss with incr
53 nflammation via hapten-specific T cells) and irritants (chemicals that are toxic to epidermal cells).
55 and bulb may provide an avenue whereby nasal irritants could affect processing of coincident olfactor
56 nasal epithelium, requiring that trigeminal irritants diffuse through the junctional barrier at the
57 ave been identified, including environmental irritants (e.g., acrolein) and ingredients of pungent na
58 (e.g., allyl isothiocyanate), environmental irritants (e.g., acrolein), and endogenous ligands (4-hy
59 nerve endings can detect certain lipophilic irritants (e.g., mints, ammonia), the epithelium also ho
61 s, microbial products and sterile endogenous irritants governs whether the outcome will be with suppr
63 vironmental and occupational sensitizers and irritants in its pathogenesis and the interaction with b
64 exposed to a range of physical and chemical irritants in the environment that are known to trigger a
66 igeminally mediated reflex reactions to some irritants including acyl-homoserine lactone bacterial qu
67 where it acts as a sensor for environmental irritants, including acrolein, and some pungent plant in
68 mediators and to a diverse array of volatile irritants, including those found in tear gas and garlic.
71 ature of bronchial asthma, and inhalation of irritants may facilitate development of nonallergic AHR.
73 , but not prevented, by elimination of local irritants, meticulous oral hygiene, and regular periodon
74 ave examined in vivo and in vitro effects of irritants, most focused on events developing hours to da
75 itial management includes avoiding causative irritants or allergens (e.g., by wearing impermeable glo
76 s) may increase the risk of LRI by acting as irritants or through increasing susceptibility to infect
77 and clears the airways and lungs of inhaled irritants, particulates, pathogens, and accumulated secr
79 ess C5aRs and that exposure to environmental irritants such as cigarette smoke modulates the expressi
82 s and responds to a wide variety of chemical irritants, such as acrolein in smoke or isothiocyanates
84 This contrasts with most other common oral irritants, such as cinnamaldehyde, capsaicin, and alcoho
87 cle beginning on page 2574), have identified irritants that activate transient receptor potential cat
90 can be activated by exogenous electrophilic irritants through direct covalent modification, we reaso
91 ized epithelial chemosensors that respond to irritants through the canonical taste transduction casca
92 vivo CM revealed corneal injury with slight irritants to be restricted to the epithelium, whereas th
93 Thus, in CF, the reduced ability of mucosal irritants to stimulate airway gland secretion via SubP m
94 , that is activated by a variety of reactive irritants via the covalent modification of cysteine resi
95 hannels are activated by chemically reactive irritants, whereas snake and Drosophila TRPA1 orthologs
96 single or multiple high-level exposure(s) to irritants, whereas this relationship can only be inferre
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