Enhanced Expression of CXCL13 in Human Helicobacter pylori-Associated Gastritis

Nakashima, Yujiro; Isomoto, Hajime; Matsushima, Kayoko; Yoshida, Akira; Nakayama, Toshiyuki; Nakayama, Masaaki; Hisatsune, Junzo; Ichikawa, Tatsuki; Takeshima, Fuminao; Hayashi, Tomayoshi; Hirayama, Toshiya; Kohno, Shigeru

doi:10.1007/s10620-011-1717-8

Cited by 20 publications

(14 citation statements)

References 28 publications

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“…Recent studies have shown that CXCL13 and IL-10 were specific markers of CNS lymphoma [27]. Nakashima et al [28] reported significantly elevated CXCL13 expression levels in H. pylori-positive patients compared with those in uninfected controls. The CXCL13 expression levels also correlated with the degree of chronic gastritis and bacterial colonization observed.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Gene Expression Between Pediatric and Adult Gastric Mucosa with Helicobacter pylori Infection

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Comparison of Gene Expression Between Pediatric and Adult Gastric Mucosa with Helicobacter pylori Infection

et al. 2015

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“…TLS resemble germinal centers of B cell follicles but lack a stable structural organization. They develop at target organs of chronic inflammatory autoimmune and infectious diseases and in the surroundings of solid tumors [5][6][7].…”

Section: Open Accessmentioning

confidence: 99%

Chemokine CXCL13 in serum, CSF and blood–CSF barrier function: evidence of compartment restriction

Pilz

Sakic

Wipfler

et al. 2020

Fluids Barriers CNS

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Background and purpose: Elevation of the chemokine CXCL13 in CSF frequently occurs during active and acute CNS inflammatory processes and presumably is associated with B cell-related immune activation. Elevation levels, however, vary a lot and "leaking" of CXCL13 from blood across dysfunctional brain barriers is a possible source. The aim was to clarify the relation between CXCL13 concentrations in CSF, CXCL13 concentrations in serum and blood-CSF barrier (BCSFB) function for a correct interpretation of the intrathecal origin of CXCL13. Methods: We retrospectively analyzed CXCL13 of banked CSF/serum samples (n = 69) selected from patient records and categorized the CSF CXCL13 elevations as CXCL13 negative (< 30 pg/ml), low (30-100 pg/ml), medium (101-250 pg/ml), or high (> 250 pg/ml). CXCL13 concentrations in CSF and serum and the corresponding CSF/serum CXCL13 quotients (Qcxcl13) were compared to CSF/serum albumin quotients (QAlb) as a measure for BCSFB function. The CXCL13 negative category included two subgroups with normal and dysfunctional BCSFB. Results: Serum CXCL13 concentrations were similar across categories with median levels around 100 pg/ml but differed between individuals (29 to > 505 pg/ml). Despite clear evidence in serum, CXCL13 was detectable only at trace amounts (medians 3.5 and 7.5 pg/ml) in CSF of the two CXCL13 negative subgroups irrespective of a normal or pathological QAlb. Moreover, we found no association between CSF and serum CXCL13 levels or between QAlb and CSF CXCL13 levels in any of the CSF CXCL13-delineated categories. CXCL13 apparently does not "leak" from blood into CSF. This implies an intrathecal origin also for low CSF CXCL13 levels and a caveat for analyzing the Qcxcl13, because higher serum than CSF concentrations arithmetically depress the Qcxcl13 resulting in misleadingly low CSF/serum quotients. Conclusion: We demonstrated that CXCL13 does not cross from blood into CSF, not even during severe BCSFB dysfunction. CSF CXCL13 elevations therefore most likely always are CNS-derived, which highlights their relevance as indicator of inflammatory CNS processes. We recommend data should not be corrected for BCSFB permeability (QAlb) and not to calculate CSF/serum quotients for CXCL13 as these may introduce error.

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“…High infiltration of CD20-positive cells has been observed in lymphoid follicles induced by H. pylori infection on immunohistochemistry. 52 No other B-cell-specific differentiation antigens have been expressed significantly more highly in pediatric antral NG than in NG-negative pediatric corpus tissue and adult AG tissue. Therefore, CD20 enrichment may result not only from a B-cell-abundant environment, but also from its role in the development of NG.…”

Section: Discussionmentioning

confidence: 96%

“…Given that CD20 is a B‐cell‐specific differentiation antigen present in most stages of B‐cell development, CD20 upregulation was expected to occur naturally in an environment rich in B cells such as GC and lymphoid follicles. High infiltration of CD20‐positive cells has been observed in lymphoid follicles induced by H. pylori infection on immunohistochemistry . No other B‐cell‐specific differentiation antigens have been expressed significantly more highly in pediatric antral NG than in NG‐negative pediatric corpus tissue and adult AG tissue.…”

Section: Discussionmentioning

confidence: 99%

Host response genes associated with nodular gastritis in Helicobacter pylori infection

Ikuse

Ohtsuka

Obayashi

et al. 2018

Pediatrics International

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Enhanced Expression of CXCL13 in Human Helicobacter pylori-Associated Gastritis

Abstract: The enhanced induction of CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis.

Cited by 20 publications

References 28 publications

Comparison of Gene Expression Between Pediatric and Adult Gastric Mucosa with Helicobacter pylori Infection

Comparison of Gene Expression Between Pediatric and Adult Gastric Mucosa with Helicobacter pylori Infection

Chemokine CXCL13 in serum, CSF and blood–CSF barrier function: evidence of compartment restriction

Host response genes associated with nodular gastritis in Helicobacter pylori infection

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