Cholecystokinin Outcome on Markers of Intestinal IgA Antibody Response
Cholecystokinin 8 (CCK8) is an entero-octapeptide that participates in crosstalk with components of intestinal immunity via the CCK receptor (CCKR), but its role in modulation of the IgA response is not fully known under physiological conditions. Male eight-week-old BALB/c mice each were intraperito...
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Published in | Current issues in molecular biology Vol. 44; no. 6; pp. 2542 - 2553 |
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Abstract | Cholecystokinin 8 (CCK8) is an entero-octapeptide that participates in crosstalk with components of intestinal immunity via the CCK receptor (CCKR), but its role in modulation of the IgA response is not fully known under physiological conditions. Male eight-week-old BALB/c mice each were intraperitoneally injected once during 7 days with CCK8, devazapide (CCKR1 antagonist), L365,260 (CCKR2 antagonist) or vehicle (sham group). In intestinal lavages, total and secretory IgA (SIgA) were determined by ELISA; in lamina propria, IgA+ B lymphocytes and IgA+ plasma cells were analyzed by flow cytometry; mRNA levels of polymeric immunoglobulin receptor (pIgR) in epithelial cells and α chain, interleukins (ILs) in lamina propria cells were assessed by qRTPCR. Regarding the sham conditions, IgA+ plasma-cell percentage and IL-2, IL-5, IL-10 and transforming growth factor-β (TGF-β) mRNA levels were either increased by CCK8 or decreased by both CCKR antagonists. For IgA/SIgA responses, IL-4/IL-6 mRNA levels were decreased by all drugs and pIgR mRNA was increased by CCK8 and reduced by L365,260. IgA+ B cell percentage and α chain mRNA levels were elicited by CCK8 and L365,260. Data suggested a presumable differential role of CCK/CCKR on the IgA-response; outcome of L365,260 on the elicitation of IgA+ B cells and α chain mRNA needs further examination. |
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AbstractList | Cholecystokinin 8 (CCK8) is an entero-octapeptide that participates in crosstalk with components of intestinal immunity via the CCK receptor (CCKR), but its role in modulation of the IgA response is not fully known under physiological conditions. Male eight-week-old BALB/c mice each were intraperitoneally injected once during 7 days with CCK8, devazapide (CCKR1 antagonist), L365,260 (CCKR2 antagonist) or vehicle (sham group). In intestinal lavages, total and secretory IgA (SIgA) were determined by ELISA; in lamina propria, IgA+ B lymphocytes and IgA+ plasma cells were analyzed by flow cytometry; mRNA levels of polymeric immunoglobulin receptor (pIgR) in epithelial cells and α chain, interleukins (ILs) in lamina propria cells were assessed by qRTPCR. Regarding the sham conditions, IgA+ plasma-cell percentage and IL-2, IL-5, IL-10 and transforming growth factor-β (TGF-β) mRNA levels were either increased by CCK8 or decreased by both CCKR antagonists. For IgA/SIgA responses, IL-4/IL-6 mRNA levels were decreased by all drugs and pIgR mRNA was increased by CCK8 and reduced by L365,260. IgA+ B cell percentage and α chain mRNA levels were elicited by CCK8 and L365,260. Data suggested a presumable differential role of CCK/CCKR on the IgA-response; outcome of L365,260 on the elicitation of IgA+ B cells and α chain mRNA needs further examination. Cholecystokinin 8 (CCK8) is an entero-octapeptide that participates in crosstalk with components of intestinal immunity via the CCK receptor (CCKR), but its role in modulation of the IgA response is not fully known under physiological conditions. Male eight-week-old BALB/c mice each were intraperitoneally injected once during 7 days with CCK8, devazapide (CCKR1 antagonist), L365,260 (CCKR2 antagonist) or vehicle (sham group). In intestinal lavages, total and secretory IgA (SIgA) were determined by ELISA; in lamina propria, IgA + B lymphocytes and IgA + plasma cells were analyzed by flow cytometry; mRNA levels of polymeric immunoglobulin receptor (pIgR) in epithelial cells and α chain, interleukins (ILs) in lamina propria cells were assessed by qRTPCR. Regarding the sham conditions, IgA + plasma-cell percentage and IL-2, IL-5, IL-10 and transforming growth factor-β (TGF-β) mRNA levels were either increased by CCK8 or decreased by both CCKR antagonists. For IgA/SIgA responses, IL-4/IL-6 mRNA levels were decreased by all drugs and pIgR mRNA was increased by CCK8 and reduced by L365,260. IgA + B cell percentage and α chain mRNA levels were elicited by CCK8 and L365,260. Data suggested a presumable differential role of CCK/CCKR on the IgA-response; outcome of L365,260 on the elicitation of IgA + B cells and α chain mRNA needs further examination. |
Author | Arciniega-Martínez, Ivonne Maciel Gómez-López, Modesto Morales-Magaña, Juan Drago-Serrano, Maria Elisa Reséndiz-Albor, Aldo Arturo Guzmán-Mejía, Fabiola Pacheco-Yépez, Judith Jarillo-Luna, Rosa Adriana Cruz-Baquero, Andrea |
AuthorAffiliation | 4 Departamento de Formación Básica Disciplinaria, Escuela Superior de Medicina del Instituto Politécnico Nacional, Plan de San Luis esq. Salvador Díaz Mirón s/n, Mexico City 11340, Mexico 1 Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina del Instituto Politécnico Nacional, Plan de San Luis esq. Salvador Díaz Mirón s/n, Mexico City 11340, Mexico; jmoralesm1707@alumno.ipn.mx (J.M.-M.); rajarillo@ipn.mx (R.A.J.-L.); mgomezlo@ipn.mx (M.G.-L.) 5 Bacteriología, Facultad de Ciencias de la Salud, Universidad Colegio Mayor de Cundinamarca, Bogotá 111311, Colombia; candreacruz@unicolmayor.edu.co 2 Laboratorio de Inmunidad de Mucosas, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina del Instituto Politécnico Nacional, Plan de San Luis esq. Salvador Díaz Mirón s/n, Mexico City 11340, Mexico; iarciniega@ipn.mx (I.M.A.-M.); aresendiza@ipn.mx (A.A.R.-A.) 3 Departamento de Sistemas Biológicos, Universidad Autónoma Metropolitana, Unidad Xochimilco, |
AuthorAffiliation_xml | – name: 1 Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina del Instituto Politécnico Nacional, Plan de San Luis esq. Salvador Díaz Mirón s/n, Mexico City 11340, Mexico; jmoralesm1707@alumno.ipn.mx (J.M.-M.); rajarillo@ipn.mx (R.A.J.-L.); mgomezlo@ipn.mx (M.G.-L.) – name: 4 Departamento de Formación Básica Disciplinaria, Escuela Superior de Medicina del Instituto Politécnico Nacional, Plan de San Luis esq. Salvador Díaz Mirón s/n, Mexico City 11340, Mexico – name: 3 Departamento de Sistemas Biológicos, Universidad Autónoma Metropolitana, Unidad Xochimilco, Calzada del Hueso No. 1100, Mexico City 04960, Mexico; mdrago@correo.xoc.uam.mx (M.E.D.-S.); fabiolagm03@gmail.com (F.G.-M.) – name: 2 Laboratorio de Inmunidad de Mucosas, Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina del Instituto Politécnico Nacional, Plan de San Luis esq. Salvador Díaz Mirón s/n, Mexico City 11340, Mexico; iarciniega@ipn.mx (I.M.A.-M.); aresendiza@ipn.mx (A.A.R.-A.) – name: 5 Bacteriología, Facultad de Ciencias de la Salud, Universidad Colegio Mayor de Cundinamarca, Bogotá 111311, Colombia; candreacruz@unicolmayor.edu.co |
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