Cystic echinococcosis is caused by the tissue-dwelling larva (hydatid) of Echinococcus granulosus sensu lato. A salient feature is this larva is being protected by the acellular laminated layer (LL), made up of mucins and calcium inositol hexakisphosphate (Ins P 6). As the parasite grows, the LL sheds abundant particles that can accumulate in the parasite’s vicinity. Although foreign particles accumulating in tissues usually cause inflammation, the LL displays adaptations for minimising various host responses, and in vivo evidence of inflammation induced by LL particles is essentially lacking. In this work, we show that LL particles injected i.p. at a dose of 225 μg dry mass per mouse cause infiltration of eosinophils, neutrophils and monocytes/macrophages as well as disappearance of resident (large peritoneal) macrophages. The calcium Ins P 6 component was dispensable for these responses. Oxidation of the mucin carbohydrates caused decreased recruitment of neutrophils but the carbohydrate-oxidized particles caused cell influx nonetheless. The control of local granulomatous inflammation is key for survival of this larva. Therefore, our results suggest that E. granulosus must deploy mechanisms to avoid excessive local build-up of LL particles (such as targeting particles to liver Kupffer cells; Infect Immun 91:e0003123) and/or to condition the recruited cells towards immune-regulatory phenotypes.