Introduction ¿ Ovalbumin (OVA) sensitization in guinea pigs induces a distinct phenotype of allergic responses, among which the asthma model is the most extensively studied. A functionally opposite phenotype is the non-responder (NR), which, despite exhibiting high levels of OVA-specific IgE and IgG1, does not develop airway obstruction or hyperresponsiveness after chronic antigen challenge. This phenotype differs from the asthma model by high expression of the laminin isoform (LN) ß2 in pulmonary smooth muscles. However, it remains unknown whether OVA sensitization induces changes in the expression of other LNs. Therefore, the aim of this study was to compare LN expression in guinea pigs with allergic asthma and NR phenotypes and correlate these patterns with distinct pathophysiological responses. Methods ¿ Guinea pigs were sensitized and challenged with OVA and divided into two groups (asthma model and NR, n = 6 per group) according to their response. A control group (n = 6) was sensitized and challenged with saline. After 12 antigen challenges at 10-day intervals, differential cell counts were performed in bronchoalveolar lavage (BAL) samples. LN expression in airway smooth muscle (ASM) and intrapulmonary vascular smooth muscle (IVSM) was evaluated by immunohistochemistry. LN presence in BAL fluid and serum was determined by ELISA. Results ¿ LN ¿1 and LN ¿2 expression increased in ASM and IVSM in the asthma model. In contrast, LN ß3 increased in ASM and IVSM of NR. LN ¿1 increased in IVSM of both phenotypes, whereas LN ¿2 remained unchanged. ASM expression of LN ¿1 and LN ¿2 correlated with antigen-induced airway obstruction and hyperresponsiveness. Serum LN ¿1 increased in the asthma model, whereas LN ß2 was elevated in NR and, to a lesser extent, in asthma. LN ß3 levels increased in serum and BAL in both phenotypes and correlated with inflammatory cell counts. Discussion ¿ Soluble serum LNs may serve as markers to differentiate antigen-induced phenotypes. LN ¿1 and LN ¿2 may contribute to ASM contraction, while LN ß3 appears to play a role in antigen-induced airway inflammation.
