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Background. Avibactam reverses ceftazidime resistance in Pseudomonas aeruginosa expressing many extended spectrum beta-lactamases when tested in broth. We examined whether similar reversal is observed against P. aeruginosa intracellular forms. Methods. Strains: reference strains; two engineered strains with basal non-inducible expression of AmpC and their isogenic mutants with stably-derepressed AmpC; clinical isolates with complete, partial or no resistance reversion with avibactam. Pharmacodynamic model: 24h-concentration-response to ceftazidime (0.01 to 200 mg/L alone or with avibactam [4 mg/L]) of bacteria in broth or bacteria phagocytozed by THP-1 monocytes, with calculation of ceftazidime relative potency (Cs: concentration yielding a static effect) and maximal relative effect (Emax: cfu decrease at infinitely large antibiotic concentrations [efficacy in the model]) using Hill's equation. Cellular content of avibactam: quantification by LC-MS-MS. Results. For both extracellular and intracellular bacteria, ceftazidime Cs was always close to its MIC. For ceftazidime-resistant strains, avibactam addition shifted ceftazidime Cs to values close to the MIC of the combination in broth. Emax was systematically below the detection limit (-5 log10) for extracellular bacteria, but limited to -1.3 log10 for intracellular bacteria (except for 2 isolates) with no effect of avibactam. The cellular concentration of avibactam reflected extracellular concentration and was not influenced by ceftazidime (0-160 mg/L). Conclusions. Avibactam potential for inhibition of beta-lactamases is not different for extracellular and intracellular forms of P. aeruginosa, denoting an unhindered access to its target in both situations. The loss of maximal relative efficacy of ceftazidime against intracellular P. aeruginosa was unrelated to resistance via avibactam-inhibitable beta-lactamases.