Research Article Mice Selected for Acute Inflammation Present Altered Immune Response during Pristane-Induced Arthritis Progression Mara A. Correa, 1 Andrea Borrego, 1 José R. Jensen , 1 Wafa H. K. Cabrera , 1 Michele Barros, 2 Iana S. S. Katz, 3 Tatiane Canhamero, 1 Monica Spadafora-Ferreira, 1 Jussara G. Fernandes, 1 Nancy Starobinas , 1 Orlando G. Ribeiro , 1 Olga M. Ibañez , 1 and Marcelo De Franco 1,3 1 Laborat´ orio de Imunogen´ etica, Instituto Butantan, S˜ ao Paulo, Brazil 2 Laborat´ orio de Imunologia Experimental, Instituto de Ciˆ encias Biom´ edicas (USP), S˜ ao Paulo, Brazil 3 Sec ¸˜ ao de Diagn´ ostico, Instituto Pasteur, S˜ ao Paulo, Brazil Correspondence should be addressed to Marcelo De Franco; mdf171717@gmail.com Received 27 July 2018; Revised 30 August 2018; Accepted 9 September 2018; Published 8 October 2018 Academic Editor: Dimitrios P. Bogdanos Copyright © 2018 Mara A. Correa et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Mouse lines selected for maximal (AIRmax) or minimal acute infammatory reaction (AIRmin) were used to characterize the immune response and the infuence of genetic background during pristane-induced arthritis (PIA). Susceptible AIRmax mice demonstrated exacerbated cellular profles during PIA, with intense infltration of lymphocytes, as well as monocytes/macrophages and neutrophils, producing higher levels of IL-1, IFN-, TNF-, IL-10, total IgG3, and chemokines. Resistant AIRmin mice controlled cell activation more efciently than the AIRmax during arthritis progression. Te weight alterations of the spleen and thymus in the course of PIA were observed. Our data suggest that selected AIRmax cellular and genetic immune mechanisms contribute to cartilage damage and arthritis severity, evidencing many targets for therapeutic actions. 1. Introduction Heterogeneous mice selected for maximal (AIRmax) and minimal (AIRmin) acute infammatory reaction are use- ful models for studying cellular and genetic mechanisms involved in arthritis susceptibility [1, 2] that may also con- tribute to the development of rheumatoid arthritis (RA) in humans. Te stages of RA are difcult to be studied in humans. Terefore, several experimental arthritis models have been developed, becoming valuable tools for comprehensive inves- tigation of the pathogenic pathways involved [3–6] and target discovery for preventive or therapeutic strategies [7]. Tese models include arthritis induced by the injection of zymosan (ZIA), adjuvants (AIA), proteoglycan (PGIA), type II collagen (CIA), or pristane (PIA) [7, 8]. Adjuvants and mineral oils have been described to induce autoimmune/infammatory syndrome in humans, resulting from a complex interplay between genetic predisposition and environment factors, as observed in many collateral efect postvaccination phenom- ena and other disorders [9, 10]. PIA has proven to be an important experimental model for RA. Te natural saturated terpenoid alkane pristane (2,4,6,10-tetramethylpentadecane) induces an acute infam- mation followed by a chronic relapsing phase when intro- duced into the peritoneal cavity. Te reaction is T-cell depen- dent with edema and articular infltration of mononuclear and polymorphonuclear cells, anti-dsDNA (double strand DNA), and anti-hsp (heat shock protein) antibodies in serum [11–14]. AIRmax and AIRmin mice were phenotype selected for acute infammation starting from a polymorphic foundation population (F0), which was established by crossing A, DBA2, P, SWR, CBA, SJL, BALB/c, and C57BL/6 inbred mouse strains. Localized 24-hour leukocyte infux and exudated pro- teins afer subcutaneous injection of polyacrylamide beads were the selection phenotypes used as phenotype indicators 24 h afer the subcutaneous injection of polyacrylamide beads Hindawi BioMed Research International Volume 2018, Article ID 1267038, 10 pages https://doi.org/10.1155/2018/1267038