Mice that express human interleukin-8 have increased mobilization of immature myeloid cells, which exacerbates inflammation and accelerates colon carcinogenesis (Record no. 51060)

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fixed length control field 03010nam a2200373Ia 4500
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control field MX-MdCICY
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control field 20250625160200.0
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Transcribing agency CICY
090 ## - LOCALLY ASSIGNED LC-TYPE CALL NUMBER (OCLC); LOCAL CALL NUMBER (RLIN)
Classification number (OCLC) (R) ; Classification number, CALL (RLIN) (NR) B-16895
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Title Mice that express human interleukin-8 have increased mobilization of immature myeloid cells, which exacerbates inflammation and accelerates colon carcinogenesis
490 0# - SERIES STATEMENT
Volume/sequential designation Gastroenterology, 144(1), p.155-166, 2013
520 3# - SUMMARY, ETC.
Summary, etc. Background Aims: Interleukin (IL)-8 has an important role in initiating inflammation in humans, attracting immune cells such as neutrophils through their receptors CXCR1 and CXCR2. IL-8 has been proposed to contribute to chronic inflammation and cancer. However, mice do not have the IL-8 gene, so human cancer cell lines and xenograft studies have been used to study the role of IL-8 in colon and gastric carcinogenesis. We generated mice that carry a bacterial artificial chromosome that encompasses the entire human IL-8 gene, including its regulatory elements (IL-8Tg mice). Methods: We studied the effects of IL-8 expression in APCmin+/- mice and IL-8Tg mice given azoxymethane and dextran sodium sulfate (DSS). We also examined the effects of IL-8 expression in gastric cancer in INS-GAS mice that overexpress gastrin and IL-8Tg mice infected with Helicobacter felis. Results: In IL-8Tg mice, expression of human IL-8 was controlled by its own regulatory elements, with virtually no messenger RNA or protein detectable under basal conditions. IL-8 was strongly up-regulated on systemic or local inflammatory stimulation, increasing mobilization of immature CD11b+Gr-1+ myeloid cells (IMCs)with thioglycolate-induced peritonitis, DSS-induced colitis, and H. felis-induced gastritis. IL-8 was increased in colorectal tumors from patients and IL-8Tg mice compared with nontumor tissues. IL-8Tg mice developed more tumors than wild-type mice following administration of azoxymethane and DSS. Expression of IL-8 increased tumorigenesis in APCmin+/- mice compared with APCmin+/- mice that lack IL-8; this was associated with increased numbers of IMCs and angiogenesis in the tumors. Conclusions: IL-8 contributes to gastrointestinal carcinogenesis by mobilizing IMCs and might be a therapeutic target for gastrointestinal cancers.
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Topical term or geographic name entry element COLON CANCER
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element GASTRIC CANCER
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element IMMUNE REGULATION
650 14 - SUBJECT ADDED ENTRY--TOPICAL TERM
Topical term or geographic name entry element MOUSE MODEL
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Asfaha, S.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Dubeykovskiy, A.N.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Tomita, H.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Yang, X.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Stokes, S.
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Personal name Shibata, W.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Friedman, R.A.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Friedman, R.A.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Dubeykovskaya, Z.A.
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Personal name Muthupalani, S.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Ericksen, R.
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Personal name Frucht, H.
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Personal name Fox, J.G.
700 12 - ADDED ENTRY--PERSONAL NAME
Personal name Wang, T.C.
856 40 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://drive.google.com/file/d/1H8E7Kummz7Ao_acHO67tXtwFFJcy9wUr/view?usp=drivesdk">https://drive.google.com/file/d/1H8E7Kummz7Ao_acHO67tXtwFFJcy9wUr/view?usp=drivesdk</a>
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Source of classification or shelving scheme Clasificación local
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  Clasificación local     Ref1 CICY CICY Documento préstamo interbibliotecario 25.06.2025   B-16895 25.06.2025 25.06.2025 Documentos solicitados