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1 -1beta or tumor necrosis factor alpha in the nasal mucosa.
2 ls (DCs) and plasmacytoid DCs (pDCs), to the nasal mucosa.
3 d to delayed clearance of influenza from the nasal mucosa.
4 cific immune responses by vaccination at the nasal mucosa.
5 regulation of type I and -III interferons in nasal mucosa.
6 t infections, its main entry route being the nasal mucosa.
7  within the nasal-associated lymphoid tissue/nasal mucosa.
8  progenitors and the formation of OEC in the nasal mucosa.
9 -mediated ion transport were measured in the nasal mucosa.
10 mRNA) and function was investigated in human nasal mucosa.
11 ivation or increased immune residence in the nasal mucosa.
12  inflammatory innate immune responses in the nasal mucosa.
13 ous system through physical contact with the nasal mucosa.
14 used by an infection and inflammation of the nasal mucosa.
15 go direct transport to brain or CSF from the nasal mucosa.
16 on their underlying biological mechanisms in nasal mucosa.
17 ples, including human cases from the lip and nasal mucosa.
18 ree different sites: lesion, non-lesion, and nasal mucosa.
19 mokines attracting inflammatory cells to the nasal mucosa.
20 y DNA methylation and gene expression in the nasal mucosa.
21  local mRNA delivery to the mouse muscle and nasal mucosa.
22 alone, induce neutralizing antibodies in the nasal mucosa.
23 by ex vivo permeation studies across porcine nasal mucosa.
24 RPV1-SP nociceptive signaling pathway in the nasal mucosa.
25 and Gammapapillomavirus have tropism for the nasal mucosa.
26  derived from cytotoxic NK or T cells of the nasal mucosa.
27 that Solutol HS15 had no toxic effect on the nasal mucosa.
28 on, which contained PBS-diluted normal human nasal mucosa.
29 e in promoting S. aureus colonization of the nasal mucosa.
30  plasmacytoid dendritic cells (pDCs), to the nasal mucosa.
31 d may also involve chromatography across the nasal mucosa.
32  as well as eosinophilic inflammation in the nasal mucosa.
33 n and a mean peak of 5.97 x 102 ng/mL in the nasal mucosa 2-3 days after infusion.
34 n, and a mean peak of 5.97x10 2 ng/ml in the nasal mucosa 2-3 days after infusion.
35 in bronchoalveolar lavage (~3.4 log(10)) and nasal mucosa (~2.9 log(10)) versus sham controls.
36 out 1 to 2% of serum AZD7442 was detected in nasal mucosa, a site of SARS-CoV-2 infection.
37 microenvironments have been described in the nasal mucosa, a site where the complex functions of olfa
38 rize the predominate immune cell type in the nasal mucosa: a resident T cell like population with pot
39 lipoprotein E (ApoE) deficiency in the N-ERD nasal mucosa affects the cross talk and inflammatory act
40  a more robust innate immune response in the nasal mucosa after infection with SARS-CoV-2.
41 )NP(366)-specific CD8 T cells persist in the nasal mucosa after primary influenza infection and predo
42 livers standardized allergens locally to the nasal mucosa allowing clinical symptoms and biospecimens
43 Additionally, the proximity of the CP to the nasal mucosa allows targeted therapeutic interventions.
44  had markedly reduced type-2 inflammation in nasal mucosa and ameliorated-nose-scratching events than
45 creases in pDC and mDC numbers at 8 h in the nasal mucosa and at 8-48 h in the skin.
46 fects of stimulation of the receptors in the nasal mucosa and carotid body chemoreceptors on vascular
47 ffects or evidence of absorption through the nasal mucosa and did not interfere with development of n
48 ninfected brain homogenate rapidly cross the nasal mucosa and enter the lumen of lymphatic vessels fo
49 wever, aged mice had fewer lymphatics in the nasal mucosa and hard palate and reduced CSF outflow to
50 mily V, receptor 1 (TRPV1) expression in the nasal mucosa and higher concentrations of substance P (S
51 R features an overexpression of TRPV1 in the nasal mucosa and increased SP levels in nasal secretions
52       The distribution of SP and TLRs in the nasal mucosa and local airway neurons was assessed with
53             The rate of viral clearance from nasal mucosa and lungs was not altered by removal of NAL
54 he severity of patients' symptoms, aspect of nasal mucosa and medical intake as parameters of CRS con
55 infection resulted in the degradation of the nasal mucosa and nasal-associated lymphoid tissue (NALT)
56 d with the induction of ICOS in cells of the nasal mucosa and on both CD4+Foxp3+ and CD4+Foxp3- T cel
57 disease characterized by inflammation of the nasal mucosa and paranasal sinuses.
58 ndication that ATS-NLCs can pass through the nasal mucosa and reach the brain or systemic circulation
59 ed the pathogen-specific IgA response in the nasal mucosa and simultaneously decreased inflammatory c
60  Gli3 is critical for OEC development in the nasal mucosa and subsequent GnRH-1 neuronal migration.
61 s, and rare epithelial tissues including the nasal mucosa and the ependyma/choroid plexus in the brai
62 light on the complex immune responses in the nasal mucosa and the periphery after influenza vaccinati
63 2A13 cDNA was prepared by RNA-PCR from human nasal mucosa and was translated using a baculovirus expr
64 mation of olfactory ensheathing cells in the nasal mucosa, and impairs GnRH-1 neuronal migration to t
65  brain, lung, liver, gastrointestinal tract, nasal mucosa, and skin.
66 ing to M cells, passing between cells of the nasal mucosa, and within lymphatic vessels of the nasal
67 ribution of adaptive response induced in the nasal mucosa appears to be key factors in generating pro
68 nce or mediate clearance of S. aureus on the nasal mucosa are fundamentally undefined.
69 d that age and immune cell proportion in the nasal mucosa are inversely correlated, with little evide
70 ver, increases in PR8-specific serum IgG and nasal mucosa-associated IgA were detected after removal
71 l of NALT did not elicit changes in serum or nasal mucosa-associated influenza-specific Ig levels.
72 terial spores, phagocytosis of spores in the nasal mucosa-associated lymphoid tissue (NALT) and lungs
73  from the cervical lymph nodes (CLN) and the nasal mucosa-associated lymphoid tissue (NALT) and teste
74 is infections have two portals of entry, the nasal mucosa-associated lymphoid tissue (NALT) and the l
75 ntly reported that GAS preferentially target nasal mucosa-associated lymphoid tissue (NALT) in mice,
76 ficking of iFT from the nasal passage to the nasal mucosa-associated lymphoid tissue (NALT).
77 llowing inoculation, but not in the adjacent nasal mucosa-associated lymphoid tissue (NALT).
78                                              Nasal mucosa-associated lymphoid tissue and submandibula
79 ce at 4 or fewer nonoverlapping areas on the nasal mucosa at the junction of the upper and lower late
80  ATS as NLCs enhanced permeation through pig nasal mucosa better than drug solution.
81           Leukocyte subsets were assessed in nasal mucosa biopsies at baseline and after treatment.
82  GFP was detected in the epithelial cells of nasal mucosa, bronchioles, and alveoli for up to 4 days
83 ophils in the superficial compartment of the nasal mucosa, but it had no effect on inflammation in th
84 ly into mice, rM51R-M virus was cleared from nasal mucosa by day 2 postinfection and was attenuated f
85 sal spray on the afferent innervation of the nasal mucosa by monitoring trigeminal nerve activity in
86          Stimulation of the receptors in the nasal mucosa caused reflex apnoea and vasoconstriction i
87 cific IgG and IgA responses in the serum and nasal mucosa compared to unmodified protein, supporting
88 an viral loads in bronchoalveolar lavage and nasal mucosa compared with after the primary infection.
89 tion two-photon microscopy studies on rabbit nasal mucosa confirmed the superior performance of TMC n
90 that causes various allergic symptoms in the nasal mucosa, conjunctiva, and skin.
91                                          The nasal mucosa constitutes the primary entry site for resp
92 wNP, compared to those isolated from control nasal mucosa (control-NM), in order to identify which ke
93                                              Nasal mucosa-derived exosomes (NMDEs) harbor immunodefen
94 ether human CD49d(+) PMNs are present in the nasal mucosa during acute viral respiratory tract infect
95                   ILC2s are recruited to the nasal mucosa during COX-1 inhibitor-induced reactions in
96 2 numbers change in peripheral blood and the nasal mucosa during COX-1 inhibitor-induced reactions in
97 marked influx of inflammatory cells into the nasal mucosa, eosinophils being the predominant cell typ
98 xia, stimulation of the sciatic nerve or the nasal mucosa evoked greater increases in SNA after expos
99 us were assessed by bacterial cell counts in nasal mucosa, fecal samples, cervical lymph nodes, and b
100 l application of short ragweed pollen to the nasal mucosa followed by a challenge of the ocular mucos
101 ar transport of inhaled pathogens across the nasal mucosa followed by entry into the lymphatic system
102 RNA is expressed at the highest level in the nasal mucosa, followed by the lung and the trachea.
103                We investigated their role at nasal mucosa following allergen challenge with house dus
104 ion of IL-4, IL-21, and IL-6 was observed in nasal mucosa following intranasal allergen challenge in
105  immunoglobulin repertoires of blood and the nasal mucosa from aeroallergen-sensitized subjects befor
106 l-transduction molecule, gp130, in olfactory-nasal mucosa from control mice and from 3-day post-OBX m
107 aucity of PrP(Sc) deposition in the oral and nasal mucosa from LRS replication-deficient hosts follow
108 5 mum between a small number of cells of the nasal mucosa in >90% of animals from 5 to 60 min after i
109 mposition and transcriptional profile of the nasal mucosa in 35 SARS-CoV-2 negative children and adul
110 n increase in ORN apoptosis or damage to the nasal mucosa in a host with a preexisting prion infectio
111    The studies shed light on the role of the nasal mucosa in active viral transmission and immune def
112  dysregulated innate immune responses of the nasal mucosa in allergic individuals may be important in
113 thways were significantly upregulated in the nasal mucosa in response to infection.
114 y, we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal sample
115 is study characterizes S. aureus adhesion to nasal mucosa in vitro and investigates the interaction o
116 LRS in prion neuroinvasion from the oral and nasal mucosa in wild-type and immunodeficient mice and i
117                   Plasma cell numbers in the nasal mucosa increased during treatment (P = .02).
118 sa and that the density of this DC subset in nasal mucosa increased significantly after in vivo aller
119                           Stimulation of the nasal mucosa increased splanchnic sympathetic nerve disc
120 , showing that the replication of VRP in the nasal mucosa induced the opening of the BBB, allowing pe
121                                     The oral-nasal mucosa is a primary site of GAS infection, and a m
122                       Here, we show that the nasal mucosa is innervated by several discrete populatio
123  indicate that acetaminophen toxicity in the nasal mucosa is not dependent on hepatic microsomal P450
124                     The influx of DCs in the nasal mucosa is not transient, as even higher numbers of
125                                          The nasal mucosa is often the initial site of respiratory vi
126            IFN-I and IFN-III immunity in the nasal mucosa is poorly characterized during SARS-CoV-2 i
127                                          The nasal mucosa is the first immunologically active site th
128 vely high prevalence of these viruses in the nasal mucosa is unknown.
129 megalovirus [CMV]) virus inoculations of the nasal mucosa leading to olfactory bulb (OB) infection ac
130  a number of extrahepatic tissues, including nasal mucosa, lung, trachea, brain, mammary gland, prost
131 e is known about lymphocyte responses in the nasal mucosa, lymphocyte accumulation in the nasal mucos
132  serum and in other compartments such as the nasal mucosa, may be required to comprehensively underst
133 m lack of olfactory ensheathing cells in the nasal mucosa, moreover, we discovered that Ascl-1 is nec
134 nasal mucosa, lymphocyte accumulation in the nasal mucosa, nasal-associated lymphoid tissue (NALT), a
135 matory responses of MSCs isolated from human nasal mucosa (nmMSCs) upon challenge with different Toll
136  RNA sequencing (scRNA-seq) to profile human nasal mucosa obtained from the inferior turbinates, midd
137 hanges in antiviral defense responses in the nasal mucosa occur in a sex-specific manner.
138 ntalized mucosal immune responses within the nasal mucosa of a vertebrate species, a strategy that li
139 ane patches decorate microcapillaries in the nasal mucosa of allergic rhinitis patients.
140 phils, mast cells and dendritic cells in the nasal mucosa of AR animals, compared with diluent treatm
141 tionally rescues the CF phenotype across the nasal mucosa of CF mice and in patient-derived organoids
142                   In addition, expression in nasal mucosa of CF mice corrected the Cl- transport defe
143               DCs were also mobilized to the nasal mucosa of children with other viral respiratory in
144                 We isolated T cells from the nasal mucosa of COVID-19 vaccinees who either experience
145 2X agonists stimulate Cl(-) transport across nasal mucosa of cystic fibrosis (CF) patients as well as
146                              The tonsils and nasal mucosa of each positive-control pig were swabbed a
147 port in human F508del CFTR lung cells and in nasal mucosa of F508del CF mice.
148 ansepithelial transport of prions across the nasal mucosa of hamsters, some of which occurs rapidly i
149 We hypothesized that immune residency in the nasal mucosa of healthy individuals may differ across th
150 E expression compared with that exhibited by nasal mucosa of healthy individuals, but APOE was inhere
151 crease in IgE(+) CD38(+) plasmablasts in the nasal mucosa of LAR patients, but not in AR or HC indivi
152  CD19(+) CD20(+) CD38(+) plasmablasts in the nasal mucosa of LAR patients.
153 esults of these studies demonstrate that the nasal mucosa of mice and hamsters is not an absolute ana
154               Amph-proteins persisted in the nasal mucosa of mice and nonhuman primates and exhibited
155 mucin release and submucosal swelling in the nasal mucosa of mice that depends on cysLTs, as it is ab
156 y infecting olfactory sensory neurons in the nasal mucosa of mice.
157 or ethmoidal nerve (AEN) that innervates the nasal mucosa of muskrats (Ondatra zibethicus).
158 okines expression was amplified in bronchial/nasal mucosa of neutrophilic asthma prone to exacerbatio
159 ials (NMPs) were measured while exposing the nasal mucosa of patients with IR and HC subjects to aero
160 at there was inflammation in portions of the nasal mucosa of the colonized mice but not in the mucosa
161            T cell accumulation peaked in the nasal mucosa on day 7, but peaked slightly earlier in th
162 required that the DNA be administered to the nasal mucosa or ocular surfaces and was not evident afte
163 ed in nasal polyp tissue but not the healthy nasal mucosa or periphery.
164 f the active medication and antigen into the nasal mucosa or to a specific effect of the active medic
165  one animal had evidence of infection in the nasal mucosa out to 23 days with associated vacuolizatio
166  in the immune cell makeup of the uninfected nasal mucosa over the lifespan.
167 rosis (CF) patients as well as across non-CF nasal mucosa, P2XRs may provide novel targets for extrac
168 as well as in vitro permeation study on goat nasal mucosa proved the superiority of the nanoemulsion
169 actors shift cellular responses in the human nasal mucosa remains uncharacterized.
170  of infection subsequent to infection of the nasal mucosa, remains elusive.
171 an viral loads in bronchoalveolar lavage and nasal mucosa, respectively, as compared with viral loads
172               Fibroblasts were obtained from nasal mucosa; samples of control subjects (NM-C, n = 8)
173 s by next-generation sequencing methods, and nasal mucosa sampling for occurrence of innate lymphoid
174 ngle-cell RNA-sequencing atlas of the murine nasal mucosa, sampling three regions during primary infl
175 ion and subsequently given IL-10 DNA via the nasal mucosa, showed diminished Ag-induced delayed type
176    Most neurons (24 of 39) were activated by nasal mucosa stimulation (+65.8 % rise in discharge rate
177 tral C1 area) greatly reduced the effects of nasal mucosa stimulation on SND (-80 %).
178    However they did not reduce the effect of nasal mucosa stimulation on SND.
179  IL-13, and IFN-gamma mRNA expression in the nasal mucosa, suggesting a mixed Th1/Th2 immune response
180 nerve-associated pathways originating in the nasal mucosa that bypass the blood-brain barrier.
181 is is a common inflammatory condition of the nasal mucosa that imposes a considerable health burden.
182 of interferon-stimulated genes (ISGs) in the nasal mucosa that is independent of the commensal microb
183  when CR9114 was administered locally to the nasal mucosa, the main mode of protection was provided b
184                                In cells from nasal mucosa, the ratio of arachidonic to docosahexaenoi
185 s well as in other structures, including the nasal mucosa, the vomeronasal organ, the epithelium of t
186 has been reformulated for application to the nasal mucosa to help reduce viral load before or after e
187  spray is forming a thin film barrier on the nasal mucosa to prevent contact with allergens, trap the
188 rate POH undergoes direct transport from the nasal mucosa to the CSF, a finding with potential signif
189 eactivity is an increased sensitivity of the nasal mucosa to various nonspecific stimuli.
190  were prepared from eight different tissues (nasal mucosa, trachea, lung, colon, intestine, pancreas,
191 observed that B cells were depleted from the nasal mucosa upon Spn colonization.
192 to test the hypothesis that prions cross the nasal mucosa via M cells.
193 dicate that prions can immediately cross the nasal mucosa via multiple routes and quickly enter lymph
194                Mean capillary density in the nasal mucosa was also approximately 5-fold higher in nas
195 t of absorption of astodrimer sodium via the nasal mucosa was also assessed in this cohort.
196 ro- and submicron particles present in their nasal mucosa was assessed.
197                                        Human nasal mucosa was cultured for 3 d with and without 1 mic
198 emic absorption of astodrimer sodium via the nasal mucosa was detected.
199                                              Nasal mucosa was immunostained for the co-expression of
200  villages on the diversity of viruses in the nasal mucosa was investigated in three Colombian village
201 t of influenza-specific CD4 T cells into the nasal mucosa was not altered by removal of NALT.
202 enge, the accumulation of CD8 T cells in the nasal mucosa was quicker, more intense, and predominantl
203               After the final challenge, the nasal mucosa was removed to produce conditioned medium,
204                      Expressions of TRPA1 in nasal mucosa were examined by immunohistochemistry.
205 ed nanoparticles enhance permeability across nasal mucosa, while retaining the effectiveness of the p
206                        Colonization of human nasal mucosa with Staphylococcus aureus sets the stage f
207 ccurred across the cribriform plate into the nasal mucosa, with a small fraction of NPs localizing wi
208  H9N2:pH1N1 (P0) virus was restricted to the nasal mucosa, with no virus detected in the trachea or l
209 that CD14(+) monocytes were recruited to the nasal mucosa within hours after local allergen challenge
210 lution, which is rapidly absorbed across the nasal mucosa without the irritation mentioned above.

 
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