Volume 120, Issue 7, Pages 1729-1736 (June 2001) Role of immunologic factors and cyclooxygenase 2 in persistent postinfective enteric muscle dysfunction in mice  Giovanni Barbara, Roberto De Giorgio, Yikang Deng, Bruce Vallance, Patricia Blennerhassett, Stephen M. Collins  Gastroenterology  Volume 120, Issue 7, Pages 1729-1736 (June 2001) DOI: 10.1053/gast.2001.24847 Copyright © 2001 American Gastroenterological Association Terms and Conditions

Fig. 1 Tension generated by muscle in response to carbachol (1 mmol/L) in noninfected control mice and in mice 28 days after T. spiralis infection. Mice were treated for 3 days after recovery from the infection with either dexamethasone 0.5 mg · kg−1 · day−1 (■) or saline (□). Age-matched noninfected controls followed the same treatment protocol. Values represent the means ± SE from each group (n = 6). **Significant difference from noninfected mice treated with saline (P < 0.01). *Significant difference from previously infected mice treated with saline (P < 0.01). Gastroenterology 2001 120, 1729-1736DOI: (10.1053/gast.2001.24847) Copyright © 2001 American Gastroenterological Association Terms and Conditions

Fig. 2 Tension generated by muscle in response to carbachol (1 mmol/L) over indicated time course after T. spiralis infection in euthymic (○) and athymic (●) mice. Values represent the means ± SE from each group (n = 4–6). *Significant difference from noninfected control tension generated for same mouse strain (P < 0.05). Gastroenterology 2001 120, 1729-1736DOI: (10.1053/gast.2001.24847) Copyright © 2001 American Gastroenterological Association Terms and Conditions

Fig. 3 (A) IL-4, IL-5, and IL-13 mRNA expression in muscle layer from noninfected control mice, mice infected at day 10, or mice infected at day 28 PI (lanes 1–3). (B) Semiquantitative expression of IL-4 (□), IL-5 (■), and IL-13 (▨) mRNA in the muscle layer from noninfected controls or mice infected 10 or 28 days PI. Values represent the means ± SE of cytokine to G3PDH ratio from at least 3 mice. *Significant difference from correspondent noninfected controls (P < 0.05). Gastroenterology 2001 120, 1729-1736DOI: (10.1053/gast.2001.24847) Copyright © 2001 American Gastroenterological Association Terms and Conditions

Fig. 4 (A) COX-2 mRNA expression in muscle layer from noninfected, acutely (day 10), and previously (day 28) infected mice (lanes 1–3). (B) Semiquantitative COX-2 mRNA expression in the muscle layer from noninfected control mice (■) and mice infected 10 days (□) or 28 days previously (▩). Values represent the means ± SE of COX-2 to G3PDH ratio from at least 3 mice. *Significant difference from correspondent noninfected controls (P < 0.05). Gastroenterology 2001 120, 1729-1736DOI: (10.1053/gast.2001.24847) Copyright © 2001 American Gastroenterological Association Terms and Conditions

Fig. 5 Representative examples of COX-2 immunoreactivity in the muscle layer of (A) noninfected control mice and (B) mice at day 28 PI. Note the marked increase in intensity of COX-2 immunostaining throughout the longitudinal and circular muscle coats of (B) previously infected mice compared with (A) controls. (C) Photomicrograph shows absence of COX-2 immunolabeling after coincubation of COX-2 peptide with the primary antibody: l.m., longitudinal muscle; c.m., circular muscle. Calibration bar, 50 mm. Gastroenterology 2001 120, 1729-1736DOI: (10.1053/gast.2001.24847) Copyright © 2001 American Gastroenterological Association Terms and Conditions

Fig. 6 (A) Tension generated by muscle in response to carbachol (1 mmol/L) in the absence (□) or presence (■) of the COX-1/COX-2 inhibitor indomethacin (1 mmol/L) control mice and mice at day 28 PI. (B) Tension generated by muscle in response to carbachol (1 mmol/L) in the absence (□) or presence (■) of the selective COX-2 inhibitor celecoxib (10 mg/mL) in control mice or mice at day 28 PI. Values represent the means ± SE from each group (n = 6). **Significant difference from muscle from noninfected mice and not exposed to the inhibitors (P < 0.01). *Significant difference from muscle from previously infected mice and not exposed to the inhibitors (P < 0.01). Gastroenterology 2001 120, 1729-1736DOI: (10.1053/gast.2001.24847) Copyright © 2001 American Gastroenterological Association Terms and Conditions