Mycobacterium abscessus, a species of nontuberculous mycobacteria (NTM), is an opportunistic pathogen that is readily cleared by healthy lungs but can cause pulmonary infections in people with chronic airway diseases. Although knowledge pertaining to molecular mechanisms of host defense against NTM is increasing, macrophage receptors that recognizeM. abscessusremain poorly defined. Dectin-1, a C-type lectin receptor identified as a fungal receptor, has been shown to be a pathogen recognition receptor (PRR) for bothM. tuberculosisand NTM. To better understand the role of Dectin-1 in host defense againstM. abscessus, we tested whether blocking Dectin-1 impaired the uptake ofM. abscessusby human macrophages, and we comparedM. abscessuspulmonary infection in Dectin-1-deficient and wild-type mice. Blocking antibody for Dectin-1 did not reduce macrophage phagocytosis ofM. abscessus, but did reduce the ingestion of the fungal antigen zymosan. Laminarin, a glucan that blocks Dectin-1 and other PRRs, caused decreased phagocytosis of bothM. abscessusand zymosan. Dectin-1−/− mice exhibited no defects in the control ofM. abscessusinfection, and no differences were detected in immune cell populations between wild type and Dectin-1−/− mice. These data demonstrate that murine defense againstM. abscessuspulmonary infection, as well as ingestion ofM. abscessusby human macrophages, can occur independent of Dectin-1. Thus, additional PRR(s) recognized by laminarin participate in macrophage phagocytosis ofM. abscessus.