Although manual and movement-based therapies utilizing tissue stretch have shown some therapeutic benefits in clinical trials of low back pain the mechanisms of these treatments and their underlying pathological substrates are poorly understood. Recently, lumbar BAY-60-7550 paravertebral soft tissues including non-specialized connective tissues have emerged as potentially important components in the pathophysiology of low back pain. Ultrasound imaging has revealed that altered thoracolumbar connective tissue thickness and echogenicity are associated with chronic low back pain, suggesting the presence of inflammation or fibrosis. Nonspecialized connective tissues in the low back of rodents have intrinsic sensory innervation and animal models show that inflammation of other types of connective tissues can be involved in the persistence of pain. In addition to its potential role in chronic pain, an important characteristic of connective tissue is its responsiveness to mechanical stimulation. In particular, recent evidence suggests that low amplitude static stretching may have beneficial antifibrotic and antiflammatory effects. The goal of this study was to investigate whether gentle stretching of tissue in vivo could reduce inflammation within the connective tissues of the low back. We first developed a novel model of non-specialized connective tissue inflammation in the rat characterized by macrophage infiltration, increased local mechanical sensitivity as well as impaired gait. We then used this model to test the hypothesis that in vivo stretching of the back twice a day for 12 days improves gait, local tissue inflammation and mechanical sensitivity. We found that carrageenan-induced inflammation of the nonspecialized connective tissues of the low back in the rat caused altered gait, increased local mechanical sensitivity and macrophage infiltration of connective tissues. All of these effects were ameliorated by tissue stretch. Our findings suggest that the nonspecialized connective tissues of the low back could be an important therapeutic target because: 1) inflammation of these tissues can cause pain and impair function and 2) the response of these tissues to a static stretch intervention could improve these outcomes. The majority of animal models relevant to low back pain have focused on injury associated with the spine. Only a few musculoskeletal rodent models have considered the contribution of connective tissue structures to pain, and no animal models so far have specifically examined inflammation of the nonspecialized connective tissues lateral of the spine. Our previous work identified and quantified calcitonin gene-related peptide expression in the nonspecialized connective tissues of the low back in control animals, indicating a potential role for these tissues in the pathogenesis of pain. This finding was supported by the work of Tesarz et al., where CGRP and substance P innervation was quantified in the thoracolumbar fascia in the rodent. In the present study we aimed to gain a greater understanding of the effects of inflammation within these nonspecialized connective tissues. A strength of the model is that it permitted us to evaluate two complementary behavioral measures: local measures of nociception and global measures of movement impairment. A limitation of mechanical sensitivity testing with Von Frey filaments is that they are applied to the surface of the skin and thus do not specifically target deeper tissues.